Clinical Neuropsychology and Neuro-Rehabilitation

Electroencephalography (EEG): Temporally Brilliant but Spatially Very Poor.

2012-02-11T12:27:00.000-08:00

Richard Caton in 1872 was first to publish a paper describing electrical activity of the brain. He found the surface of the brain showed negative voltage when activated. EEG is a modern technique used to represent electrical activation states by depicting variations in frequency and amplitude on a graph. The sleep-wake cycle provides a common depiction of different frequencies and amplitudes of signal dependent upon brain states of alertness.

Biological electricity is dictated by different concentrations of ions, ions that are disolved in solutions. It is a truism that if you separate differing ion solutions and have some sort of membrane separating them an electrical charge will be produced. Similarly, if you separate fresh water from salty sea water separated by a membrane has been used as a form of clean energy production. Within the brain, inside and outside the cell there are ion imbalances of sodium and potassium. Essentially if a neurone is excited, there is a current influx (usually of sodium) and an action potential is produced. Action potentials can be generated at very high rates. These rates are compatible with synchronous activity. Most of what EEG measures is excitatory post synaptic potentials rather than inhibitory post synaptic potentials.

Much of the scalp EEG is thought to reflect extracellular ionic changes associated with post synaptic potentials. The direct contribution of action potentials is much smaller and very short lived. What EEG really measures is much more to do with the direct consequence of the build up of ions in the extracellular space and this accounts for 15% of brain volume only. Thus activity within the brain cells influences ion concentrations in extracellelar space and this is why EEG more directly reflects brain activity than other imaging techniques that measure blood flow or metabolic activity.

Electrical activity essentially travels at the speed of light, therefore meaning the temporal resolution of EEG is effectively instantaneous. This means that EEG's best attribute allows for dividing cognitive processes into stages of very close temporal proximity (see strengths section later). This is particularly clinically useful in determing if bottom up processes are impeded, reflecting brain stem dysfunction in MS for example.

Voltage detection relies upon proximity; the inverse square law means that electrical activity decreases increasingly the further away the electrode is from the source. EEG measures voltage at regions of interest in comparison to neutral regions (for instance by placing an electrode on the ear lobe). The differential amplifier measures this discrepancy in voltage. EEG amplifiers have high and low frequency filters which act a little bit like treble and bass adjusters on a stereo. These filters help turn down the distractions from information of interest. Wavelet and fourier analysis provide further methods of understanding EEG data.

The neo cortex can be divided into six sections. Shallow layers tend to be cortico-cortical connections and alertness projections from the thalamus whilst deep layers tend to be associated with outputs from the cortex (eg cortico-subcortico projection). Neural activity is of course, both excitory and inhibitory. Pyradimal neurons straddle layers of the neo cortex. Pyramidal cells tend to orientate in the same direction and can be likened to trees in a wood. Pyramidal neurons of the cortex are thought to produce the most EEG signal because they are well-aligned and fire together.

One of the key drawbacks to EEG is not only the limiting factor of proximity in imaging subcortical activities, but also in measuring radial structures in the brain. Radial structures such as the hippocampus are structures that do not tend to have aligning neurones and therfore the electrical output tends to cancel itself out. Only consistent activity across populations of aligned neurons is recorded at the scalp. Random activity associated with randomly aligned dipoles cancels out and is not measured. This is why vertically aligned pyramidal neurons are thought to dominate scalp EEG. However, the brain is not flat and therefore this limits the spatial resolution potential of EEG. Accuracy of source localisation marginally improves with the increased amounts of electrodes on modern EEG equipment; nevertheless the bulk of EEG reflects cortical activity and only marginally reflects subcortical activity. That is not to dismiss that there is an indirect relationship to subcortical process when one considers the projections that go to the neocortex from the thalamus.

Signal averaging across event related potentials reduces noise and random artefact by using a technique that relies upon repeating stimuli over and over again and determining the signals of interest over random signals. The amounts of repeated trials is somewhat dependent upon the amplitude of the signal versus the amount of background noise, but this technique has been used effectively to divide previousely undividable cognitive process into stages.

One of the key limitations to EEG Is that the measurement is prone to both biological and environmental artefacts (factors that intefere with true signals). Mains electric supply, mobile phones and electrical devices such as computer monitors are particularly problematic environmental artefacts particularly as they are so common in hospitals and research laboratories.

Common biological artefacts include all types of muscle activity such as muscle tension, gritting teetch etc, sweat, blinks, when the tongue touches the roof of the mouth. Often biological artefacts results in high frequency artefacts, whilst environmental artefacts result in low frequency artefacts.
Best recordings should be obtained when partcipants are calm and relaxed, room temparature is comfortable and stable, no hair product is used and electrical shielding is available.

Closely related to EEG is Magneto-Encephalography (MEG). Whenever there is a difference in electrical potential, a magnetic field exists around such a difference. Magnetic north pole aligned is based upon the 'right hand rule' whereby the direction of the fingers represent the direction of current and the thumb (pointing upwards) represents the direction of the magnetic force. MEG is based upon the same principle within the brain and it is a technique that measures magnetic fields in the brain. Scalp electrical potentials that produce EEG are generally thought to be caused by the extracellular ionic currents, whereas MEG signals are more closely associated with intracellular ionic currents. EEG can be recorded at the same time as MEG so that data from these complementary high-time-resolution techniques can be combined.

Strengths of EEG and MEG:

Primarily reflects neuronal activity and associated glial activity (artefact aside)

Easy to record and relatively inexpensive

Very useful in clinical settings (identifying epilepsy and titrating treatment approaches, identifying slow function in MS and ascertain awareness/brainstem function in coma)

Very sensitive to minor changes in arousal and especially good at illustarting the sleep-wake cycle

Superb temporal resolution to millisecond level (essentially limitless)
-ability to fractionate components of cognitive activity (eg early brainstem v later cortical responses)
-ability to track brain changes which occur as a stimulus is processed in real time (perception, central processing, response preparation)
-thus EEG studies have clarified psyChodynamic models of unconcsious processes
-sensitivity to fluctuations in attention during stages of stimulus processing
-can use randomised designs as opposed to block designs

Can be analysed in real time but signal averaging removes artefact and adds great power by increasing signal to noise ratio of time-locked cognitive processing

Relatively good value in comparison to other techniques

Drawbacks of EEG and MEG:

Very poor spatial resolution.

2D representation of a 3D brain.

Largely limited to neocortical activity.

It is constantly susceptible to a number of biological and environmental artefacts, including muscle movements, seating, electrical activity nearby etc.

The inverse problem means that real electrical activity that is not aligned directionally in the tissue goes unmeasured and instead cancels itself out.

Source localisation algorithms are complex and problematic and have to make simplifying assumptions.

The meninges, cerebrospinal fluid and skull "smear" the EEG signal, obscuring its intracranial source. Furthermore the orientation of brain relative to scalp makes source localisation less reliable (although in MEG, MRI scans can be incorporated for computer analysis to compensate for size and shape of the brain in question).

This final point is perhaps a point to conclude on, that all imaging techniques have their pros and cons and that the future is perhaps about combining techniques for converging information in order to infer function of the brain.

How does Positron Emission Tomography (PET) work and has it had its day?

2012-02-04T11:20:00.000-08:00

Tomography comes from the latin 'tomo-to slice' and 'graphy- to image'. The essence of PET is to create artificially radioactive substances and introduce this to the body to be studied through the process of metabolism. The key requirement is that this radioactive material permeates the 'blood-brain barrier'. Radioactive sugar fluorodeoxyglucose (FDG) is commonly used. However, radioactive forms of drugs, neurotransmitters, gabba, serotonin and dopamine amongst other things can be used and studied with PET and this illustrates a key advantage when compared to its closest rival fMRI.

The introduction of radioactive substances to the body is usually done intravenousely, but can be accomplished through inhalation. Once inside the body the radioactive substances undergo decay and emit radioaction. This radiation is detected by the scanner (essentially a complex set of cameras) and this allows metabolically active regions of either the body or the brain to be identified. But it is important to conceptualise this as activity rather than activation. For instance the inhibition of neural systems often requires energy.

PET is not a technique for providing adequete structure. You need another form of structural imaging such as MRI or CT to provide this and then overlay the PET image to indicate function. This introduce further costs and administrative complications. Partial rotating systems go some way to addressing this criticism by saving money and provide additional room for a CT scanner within the PET scanner.

A further drawback of PET scanning is that the costs are not limited to the machine itself. A synthesis device or cyclotron is the contraption used in the production of PET isotopes to be introduced to the brain or body to be studied. The machines work by using rapid magnetic field reversals that excite particles under high energy spinning. These essentially spin out of the device and bombard a non-radioactive element which in turn produces the isotope. Often these devices are very expensive (often more expensive than the scanner itself). Furthermore there is a cost implication to the human skills and security measures needed to run these devices safely.

To understand PET one must start at the level of atom. A positron is an anti matter electron; identical to an electron but with a positive charge rather than negative. In PET positrons are produced as a result of nuclear decay. Positrons are produced by positron emitting radioisotopes. If a nucleas is unstable with too many protons it has a positive charge. Decay occurs when a proton is converted into a neutron, making the nucleas stable again. Emitted positrons only travel a short distance until they meet an electron. The distance travelled is dependent on the energy of the positron. Emitted positrons have a brief life. When matter meets anti matter you get a mutual annhililation. At the point of mutual annhilation two gamma rays (aka photons) are discharged in an opposite direction at 180 degrees to each other. This opposite direction is virtually perfectly opposite and this is very important in understanding PET scanning. The rate of decay is often quantified by 'half-life'. Differing isotopes have different half lifes and the choice of which to use depends upon the purpose of the PET investigation.

The production of gamma rays can be analogised as being like bullets being fired from a gun. A bullet flies in a straight line. Imagine a bullet blasts through a door and comes to rest in a wall. One could trace the shooter of the bullet by tracing a line back from the bullet in the wall through the hole in the door. The scanners in a PET machine are advanced enough to determine a single annihilation event by detecting both opposing sides of the gamma ray emission. The scanner can then trace the source of the annihilation to a position in three dimensional space. This is essentially the process by which the camera detects and reconstructs the image to help image the function of the body or brain. The gamma ray detectors in the PET scanner uses scintillators that involve photomultipliers to amplify the weak light emitted. Computer modelling helps reconstruct the data into a visually meaningful form.

PET scanners work on the basis that gamma rays emit at 180 degress? However there is a small natural variation. This natural variation introduces another small factor affecting resolution accuracy. Additional interference comes from both the short distance and non-linear directions travelled by the proton and rare occassions where the scanner mistakes true event annihilations from various types of random, scattered or suprious gamma ray errors.

There are various ways of controlling for error. Firstly, 2D PET rather than 3D PET are scans that deploy 'blinkers' that are often made of lead and work to restrict the span of gamma rays available, therefore improving the percentage of true annihilations, therby reducing scatter and random coincidences.

There are also specific methods for controlling random annihilation interference. The delayed window procedure corrects by shifting the time of one side of the detector by a small amount of time. The data is reanalysed and in theory every coincidence should be random. So the amount of randoms can be superimposed, counted and compared to the original amount providing an estimate of the accuracy of the scan.

Another source of inaccuracy are the scanners themselves. The crystals in the scintillators are not identical in thickness for example. To control for this the scanners are regularly calibrated. The procedure to do this involve inserting a simple radioactive rod or similar. Furthermore, there is the factor of 'dead time' which is the very short lapse of time where the scintillator has detected a gamma ray and is ready to detect another independent gamma ray. The technique depends on as low as possible amounts of radiation to control for some of this limitation.

Scatter events, whereby a gamma ray deflects off of something unrelated to that under observation, are quite rare events in comparison to true events. In 2D scans there presence is even rarer. Scatter correction presents a control method whereby events are plotted and outliers are subtracted.

Attentuation correction is an important correction procedure and it compensates for the occassions where gamma rays lose energy through collisions with extraneous particles and are therefore failed to be detected. The procedure is a calibration procedure developed from inserting a radioactive rod inserted into dummy patient/deceased body. These corrections take place in the post hoc image period.

In summary the image reconstruction requires:
A data file for all response detected within time window
A normalisation file
Two attenuation correction files
And a CT scan

Advantages of PET:

Many different tracers can be used enabling analysis of glucose, oxygenation, neurotransmitters, peptides. They can target the effects of drugs.

There is no echon planar noise, making them suitable for auditory studies (fMRI is not suitable).

High magnetic fields in fMRI machines can produce internal heat and induce currents within tissue. They are therefore applicable to those with metal objects within their bodies such as pacemakers.

PET is a measure of neural tissue rather than vascular tissue. And therefore is a reliable way of imaging certain regions where fMRI is not as accurate.

There is the exciting potential to conduct dual tracer PET involving two tracers with differing half lifes. For example, this allows an image that can detect two neurotransmitters at once.

Radioactive Gene insertion therapy can be studied.

Can be used to detect early brain area dysfunction in dementia, before any structural changes emerge.

PET has been instrumental in researching and monitoring cancers in the body.

Disadvantages:

Very poor temporal resolution is its biggest weakness compared to fMRI and EEG (many minutes to acquire scan). Hence the need for block designs, whereby people repeat an intervention in order for the scan to detect the change.

Extremely costly (scanners, security, physicists, set up costs approximatelymtwice the cost of fMRI)

Poor spatial resolution (5-7mm although improving with modern scanner 2mm has been proposed)

Some parts of the brain pulse (brain stem especially) this again interfers with resolution (although can be controlled for taking images between heart beats)

Convincing participants to consent to treatment/research is often problematic.

Conclusion
In summary, like all neuroimaging techniques, PET has recently come under scrutiny for the statistical levels at which results and conclusions are founded (Savoy 2001). Like fMRI average data will often produce different arguments than individual data. Often the number of areas identified in research increase with average data and researchers in the past have been culpable of 'fishing for data' and making unjustified or speculative post hoc hypothese.

PET on its own has had a greater research history than clinical history. For example, PET has repeatedly been used in experimental designs to illustrate the activation of thalamus and primary somatosensory cortex areas in response to pain. It's directly clinical value is severely restricted by its costs.

No single neuroimaging technique is unanimousley superior and so PET has not had its day. In fact its use has experienced somewhat of a revival since the movement away from: 'do this task, this area lights up'. Neuropsychology has moved on from a 'modern phrenology' to something more interactional and system based. Perhaps a converge of techniques is the future?

The Principles of Psychopharmacology

2012-01-18T04:11:00.000-08:00

Psychopharmacology is the study of the actions of drugs and their effects on mood, sensation, thinking, and behavior. It is the sometimes approximated as the study of drugs used in the treatment of psychiatric disorders. Psychoactive drugs in a recreational or a clinical context differ only in context, aims and ethics. They do not differ in their action.

A historical appreciation of drugs helps contextualise the long standing use of drugs in altering consciousness, extending thousands of years stemming back to the use of mushrooms in tribal rituals, for example. In a clinical context, drugs first came to be used in the mid twentieth century to treat psychiatric disorders such as depression and psychosis.

Pharmacokinetics refers to the movement and time course through the body. It is divided into several areas including the extent and rate of absorption, distribution, metabolism and excretion. This is commonly referred to as the ADME scheme:
• Absorption - the process of a substance entering the blood circulation.
• Distribution - the dispersion or dissemination of substances throughout the fluids and tissues of the body.
• Metabolism (or Biotransformation) - the irreversible transformation of parent compounds into daughter metabolites.
• Excretion (or Elimination) - the elimination of the substances from the body. In rare cases, some drugs irreversibly accumulate in body tissue.

Absorption can be done oral, rectal, transdermal, subcutaneuos, sublingual, lingual and intramuscular. The specifics of this are decided based on feasibility, absorption rate, tolerability, safety and invasiveness.

The 'blood-brain' barrier is there to protect us as a huge amount of blood needs to service the brain and a flood of something psychoactive or neurotoxic could be devastating without filter protection. Drugs therefore need to transpose the 'blood-brain barrier' and either need to be compatible with the transport system, lipid soluble, or they have to be small so that the drugs can pass successfully through it. Heroine and morphine provide a synonymous example once within the brain, but the way they are absorbed is very different, thus giving them different potencies.

Half life can be used in various domains. It usually refers to the ‘elimination’ half life. This means the half life for half of the drug to be completely metabolized. Half life is important to achieve steady state concentration. This allows for us to get to efficacious doses without reaching toxic levels or overdose.
The psychopharmacological industry have developed several mathmatical models to help determine doses and pharmacokinetic profiles of drugs. Dose-response relationships will differ across individuals, due to individual differences. Drugs will have a number of effects, each with their own dose-response relationship. Similar drugs, even with similar mechanism of action will differ. Drugs will have a phlethora of effects: Wanted effects and side effects. Sometimes the metabolites will have the effect you are interested in and it is this that dose-relationship needs to focus on.

Figure 1. Dose-Response Relationship

Two abbreviated terms are important in pharmacokinetics. ED50 refers to concept that 50 percent of the population experience efficacious doses at this level. LD50 refers to the concept that 50% of the population die at this dose (lethal). The larger the window between the two figures, the safer the drug. LD50 divided by ED50 gives therapeutic index- the ratio of safety in other words. Indexes of around 100 are considered safe.

Pharmacodynamics refers to the process by which drugs work and take effect, there mechanism of action. There are 7 main drug actions:
• stimulating action through direct receptor agonism and downstream effects
• depressing action through direct receptor agonism and downstream effects (ex.: inverse agonist)
• blocking/antagonizing action (as with silent antagonists), the drug binds the receptor but does not activate it
• stabilizing action, the drug seems to act neither as a stimulant or as a depressant (ex.: some drugs possess receptor activity that allows to stabilize general receptor activation, like buprenorphine in opioid dependent individuals or aripiprazole in schizophrenia, all depending on the dose and the recipient)
• exchanging/replacing substances or accumulating them to form a reserve (ex.: glycogen storage)
• direct beneficial chemical reaction as in free radical scavenging
• direct harmful chemical reaction which might result in damage or destruction of the cells, through induced toxic or lethal damage (cytotoxicity or irritation)

The clinical trials process is a thorough process, that is often completed over a number of years across multiple sites. They are often very specific, typically beginning with animal testing, and ending with human testing. In the human testing phase, there is often a group of subjects, one group is given a placebo, and the other is administered a carefully measured therapeutic dose of the drug in question. After all of the testing is completed, the drug is proposed to the concerned regulatory authority and is either commercially introduced to the public via prescription, or deemed safe enough for over the counter sale. Specifically, phases consist of:

Phase 1- small (20-80) test of experimental drug to determine safety, dosing and identify side effects.
Phase 2- larger (100-300) safety and efficacy
Phase 3- large scale (500+) efficacy within target population, monitor side effects and compare standard treatments.
Phase 4- Licence studies to provide further information and detail on risk and efficacy.

Figure 2. Drug Development Process

MRI and fMRI in a Nutshell

2012-01-14T13:06:00.000-08:00

MRI (AKA nuclear magnetic resonance imaging (NMRI) or magnetic resonance tomography (MRT) is a medical imaging technique used in radiology to visualise detailed internal structures. MRI makes use of the property of nuclear magnetic resonance (NMR) to image nuclei of atoms inside the body. It is a particularly useful clinical and research tool for imaging soft tissue such as the brain and has been harnessed in clinical research to support anatomical changes in syndromes such as autism, schizophrenia and severe depression to name but a few. One almost cliche study utilised MRI to establish anatomically changes in the anterior and posterior hippocampal structures in London taxi drivers (Gur et al. 200). It is routinely used in clinical practice in the detection of acquired brain injuries, such as tumour, stroke and TBI.

In order to understand how it works, it is necessary to summarise the atom. On its smallest scale the world is made up of atoms. Atoms consist of protons, neutrons and electrons that orbit or ‘spin’. Atoms with an uneven number of protons and neutrons have a 'net spin'. When atoms are outside of an MRI scanner the alignment of these net spins is randomly ordered. Under a magnetic field, they tend to align in parallel or anti-parallel. The MRI is a very powerful magnet, 30,000 times more power than the Earth’s natural polar magnetic field. Another magnetic field, the gradient field, is then applied to kick the nuclei to higher magnetization levels, with the effect depending on where they are located. When the gradient field is removed, the nuclei go slowly back to their original states (AKA relaxation), and the energy they emit is measured with a coil to recreate the positions of the nuclei. MRI thus provides a static structural view of brain matter. Magnetic field gradients cause nuclei at different locations to rotate at different speeds. By using gradients in different directions 2D images or 3D volumes can be obtained in any arbitrary orientation. Sagittal, coronal or horizontal slices can be obtained. Black areas on the scan represent no signal and white areas represent a signal (positive charge).

The brain is 70% water and water is a compound substance made up of hydrogen and oxygen elements. Hydrogen molecules are intrinsically magnetic and water concentration differentiates through different types of brain matter. MRI uses this to construct a grey scale image. For instance cerebrospinal fluid has very high water content and tumour and bone is very dense and low in water content. Images can be T1 or T2 weighted by changing the parameters of 'relaxation' time. White matter appears in a light grey in T1 and a dark grey in T2. Grey matter appears grey in both and cerebrospinal fluid (CSF) appears black in T1 and white in T2. T1 and T2 weighting is a helpful option in clinical scenarios where one type of matter is particularly important to identify (the extent of a tumour for example).
Exciting new techniques involving the introduction of high contrast agents are currently in development. They have some contraindications to health but they have now been approved for specific uses in clinical research and practice.

Functional magnetic resonance imaging or functional MRI (fMRI) is an MRI procedure that measures brain activity by detecting associated changes in blood flow. The primary form of fMRI uses the blood-oxygen-level-dependent (BOLD) contrast, discovered by Seiji Ogawa. The central thrust behind fMRI was to extend MRI to capture functional changes in the brain caused by neuronal activity. Differences in magnetic properties between arterial (oxygen-rich) and venous (oxygen-poor) blood provided this link. When neurons become active, local blood flow to those brain regions increases, and oxygen-rich (oxygenated) blood displaces oxygen-depleted (deoxygenated) blood. In a nutshell deoxygenated hemoglobin is more magnetic than oxygenated hemoglobin, which is virtually nonmagnetic. This difference leads to an improved MR signal since the nonmagnetic blood interferes with the magnetic MR signal less. This improvement can be mapped to show which neurons are active at a time.

fMRI is used to often used in avoiding key functional areas of the brain in prepartion for surgical or other invasive intervnetion. It is also often used to anatomically map the brain and detect the effects of tumors, stroke, head and brain injury, or degenerative diseases such as dementia. Research use is ahead of clinical use, mainly becuase clinical populations present logistical or ethical complications to scanning (scanning a child with ASD, with communication difficulties who require informed consented is an illustration of a collection of these difficulties). Despite this, in addition to the uses of MRI, fMRI has been used clinically to map functional areas, check left-right hemispherical asymmetry in language and memory regions, check the neural correlates of a seizure and test how well a drug works.
Like any technique, fMRI has advantages and disadvantages, and in order to be useful, the experiments that employ it must be carefully designed and conducted to maximize its strengths and minimize its weaknesses.

-Advantages-
-It can noninvasively record brain signals without risks of ionising radiation inherent in other scanning methods, such as CT or PET scans.
-It has satisfactory spatial resolution, particularly in collaboration with a normal MRi scan.
-It can record signal from all regions of the brain, unlike EEG/MEG, which are biased toward the cortical surface.
-It has led to major new understandings of human function, particular in light of real-time intervnetion studies.

-Disadvantages-
-The BOLD signal is only an indirect measure of neural activity and, as described before, could be influenced by elements other than the experimental manipulation (disease, sedation, anxiety, medications that dilate blood vessels, and attention (neuromodulation).
-BOLD signals reveal input rather than output and one isn't necessarily the other.
-The technique has been criticised for its poor temporal resolution. The BOLD response peaks approximately 5 seconds after neuronal firing begins in an area. While interleaved stimulus presentation can increase temporal resolution, it correspondingly reduces the data points collected.
-While the static magnetic field has no known long-term harmful effect on biological tissue, it can cause damage by pulling in nearby heavy metal objects converting them to projectiles.
-The most common risk to participants in an fMRI study is claustrophobia. But people with pacemakers are catastrophically at risk on entering a scanner.
-The scanner is very expensive.
-The costs mean that clinical practice has lagged behind privately funded research.
-fMRI research statisitcal methods have recently fallen under strutiny, thereby questionning past findings.

“Cognition does not Exist in a Vacuum”

2012-01-12T10:53:00.000-08:00

Before the 18th century people generally thought that the heart was responsible for emotions and thoughts. This sounds bizarrely impressive given what we know now, but remnants of this still exist with the metaphorical representation of the heart in its connection with the emotion of love. But people really once hypothesised that the heart did precisely what the brain does. The first record of a dissenting opinion on this came in the early 1700’s. Gall is renowned for his 18th century theory of “phrenology”. This theory explained how the shape of the skull, as a dictation of the shape of the brain, predicted various attributes. One could feel their way across the skull and detect the likelihood of barbarianism and other antiquated characteristics. Of course by modern standards his theories are almost entirely rubbished. However, almost by coincidence he was on the right path.... or was he?

Flouren’s 19th century animal lesion studies were the next landmark breakthrough in use of detailed behavioural analysis to study the underlying functions of the brain. Following this, names such as Kleist and Lashley made important contributions in identifying function based upon localisation of brain injury/lesion. A key 20th century case-in-point is Miller’s patient “M”, who experienced catastrophic lesion of the hippocampus during surgery. He suffered profound amnesia as a result, meaning he could not consolidate and store memories at all. For a slightly more up to date collection of evidence based lesion studies, Damasio provides a key text outlining what we now know about the localisation of brain function.
Lesion based research, is however, not without its criticisms. Firstly, it says little of functional systems and pathways. It explains little of individual difference and secondary impact of brain injury/lesion. Furthermore, as research gathered pace through history, researchers began to move away from a simplistic view of ‘tissue location=specific function” and began to recognise the inter-related relationships and systems that contribute to human brain function.

Alongside these key historical developments of localisation theory the levels at which we understand the brain have developed and evolved. Nowadays we try our best to understand the brain in terms of anatomy, chemistry, activity, function and behaviour. We have 52 distinct anatomically distinct areas dictated by conceptually useful approximate function and interrelatedness (see Brodman’s 52 areas). This has led to many benefits in helping those who have experienced neurological insult in their rehabilitation and planning, not to mention, helping guide neurosurgeons in avoiding damage to key language areas of the brain during surgery.

But let’s return to heart, or perhaps better still, Gall’s “phrenology”. There is a risk that modern imaging methods may fall into a similar trap to Gall. Collectively, and quite possibly to our detriment, we are very eager to discover more about mankind and his workings. The assumption of dysfunction equalling lesion is a faux pas made even in modern times, with the advent of modern structural and functional imaging research and for use in clinical enquiry. Recent research suggests that MRI research in particular should be reviewed and more conservative statistical procedures be deployed (see Vul et al. 2009). The brain is a wonderfully complex organ that demands a commensurate ways of understanding it. Later in my blogs I shall attempt to summarise modern structural and functional imaging techniques in order to illustrate how this history of human curiosity continues.

Orientating Around the Brain

2012-01-10T10:28:00.000-08:00

The following technical terms are used to orientate around and within the brain and its structures:

Top=dorsal/superior
Bottom=ventral/inferior
Front=rostral/anterior
Back=caudral/posterior
Medial=mid-line
Lateral=away from mid-line
Contralateral=opposite side as
Ipsilateral=same side as
Unilateral=one side only
Bilateral=both sides
Proximal=close
Distal=distant

MUS and Neuropsychology

2011-12-27T11:19:00.001-08:00

What Can Neuropsychology Contribute to the Identification and Treatment of Medically Unexplained Neurological Symptoms?

Medically Unexplained Symptoms (MUS) is an umbrella term for a broad collection of symptoms and syndromes that physical processes alone fails to explain. It has been criticised as type of 'non diagnosis' as it essentailly diagnoses what it is not rather than what it is. However, the term has gained popularity over other terms, such as cogniform disorder or somatisation because patients tend to view it as non-threatening, and because positive relationships to professionals (usually the GP) are a key correlate to positive outcome. Examples of MUS phenomena arguably include: inexplicable pain, inexplicable headache, fibromyalgia, chronic fatigue, and non epileptic attack disorder.

Up to one in five GP appointments is MUS related. It is important to statistically contextualise prevalency as sometimes medical experts are wrong and up to 5% of those diagnosed with MUS subsequently turn out to be medically explainable cases following long term follow-up. However, a mixture of factors including: a growth in civil prosecution, an increase in 'blame culture' and the advent of patient internet derived knowledge, has meant medics have approaches MUS with relentlessly fruitless further medical investigations. The costs and harms both physically, psychologically and financially of this trend is worrying and has attracted attention from psychologists and neuropsychologists alike.

The contribution clinical psychology and neuropsychology can make to MUS sufferers is at two levels: identification and treatment. Where complaints are made of a neurological nature symptom validity tests (SVTs) are routinely used in neuropsychological assessment to identify MUS. They are particular useful in questions over whether a patient has infact sustained a mild head injury or whether they are:
1 Completely malingering
2 or either consciousely or unconsciousely exaggerating symptoms

The BPS now advise routine use of SVTs even in clear cases of organic pathology, primarily to substantiate the reliability of test results and clinical interpretations. Each SVT has it's strengths and weaknesses. Each test aims to strike an appropriate balance between the likelihood of making type 1 versus type 2 error. Each test essentially aims to identify those who are making less than maximum effort. Similarly, 'forced choice' tests, tests that even when completed by random chance stand a 50% correct level, specifically aim to identify those who deliberately aim to mislead testers. Psychological assessments of personality and psychopathology can also be used as an adjunct in correctly identifying MUS. Subscales indicating anxiety, depression, somatisation, neuroticism and exaggeration of symptoms are often used as indicators of potential MUS. Unusual symptoms, symptoms out of context, long histories of attendance at A&E/GP are other indicators of increased MUS likelihood (see previous blog on DSM-IV indicators).

Most often psychological factors play a central explanatory role. It is believed approximately 70% of MUS patients share comorbidity with psychiatric symptoms, most often anxiety and depression, although the extrapolation of cause and effect complicate this simplistic statistic. At the level of treatment psychologists offer evidence based 'talking interventions' such as CBT and associated approaches. Such approaches focus upon: treating anxiety and depression symptoms, encouraging patients to acceptance their scenario and their symptoms, symptom management and dissemination of psychological formulation as an explanation of symptoms.

Psychologists have become increasingly interested in being involved at the primary care level. In Devon, Plymouth began a pilot project in 2008 focussing upon scripting GP messages on initial MUS diagnosis, specific risk assessment for MUS patients and approaches aimed at minimising unneccessary and potentially harmful medical investigations. Psychological approaches have identified the importance in 'getting in early'. Clinicians and researchers have identified a 6 month critical period for intervening (Bass/Stone/Halligan). Beyond this outcomes become increasingly pessimistic. MUS unsurprisingly fall into three crude groups, of which research is in process: 1. Those who are treatable; 2. Those who may become treatable; and 3. Those who will be highly resistant. Psychologists with considerable MUS experience will usually know which group a patient fits into following the first or second session.

A Neuropsychological Understanding of Anxiety

2011-12-20T08:00:00.000-08:00

Anxiety is conceptually closely aligned with fear and stress responses and the concept of arousal level. As with most emotional topics concerning the brain the amygdala is implicated in all of the anxiety disorders (Etkin and Wager, 2007).

Within the lierature there is a lateralisation theory of the amygdala. The left amygdala is chiefly responsible for sustained emotional evaluation and the right short and rapid emotional stimuli detection (Phelps et al 2001; Baas et al. 2004). It is now believed past studies have neglected and dismissed right amygdala activation because of older technologies that used lower temporal resolution.

Stein et al. (2007) provides more up to date fMRI evidence for amygdala activation as described above in anxiety prone individuals versus controls. Further studies have noted gender differences, including increased left activation in war veterans with PTSD diagnoses (Shin et al. 2004). It is possible that this can be explained by gender differences in how emotional memories are constructed: language based-left-female; visual based-right-male.

The anterior cingulate cortex is responsible for motor control, cognition and arousal/drive state. Essentially it is involved in translating intentions into actions and in popular metaphor it is implicated in 'fight or flight' responses.
Lesion studies have revealed arousal dysfunction in the absence of other neuropsychological dysfunction.

The dorsomedial prefrontal cortex has an anxiety inhibiting function when active. Kalisch et al. (2004) evidenced trait anxiety correlations to DmPfC function through animal studies and Etkin (2007) mirrored such findings in human lesion studies. Lesions in the DmPfC tend to flatten anxiety responses although findings are inconsistent and there are methodological limitations to the evidence base.

The ventromedial prefrontal cortex has a top down inhibitory effect upon the amygdala. fMRI evidence shows hypoactivation of VmPc when anxiety is high; thus there is a negative correlation to amygdala activity and PET studies have triangulated this finding (Ahs et al. 2009). In theory amydala lesion would necessitate a lower likelihood of developing anxiety and VmPfc lesion would predict an increased likelihood of anxiety development. However, the evidence base is somewhat contradictory, perhaps providing conceptual support for an emotional regulation model rather than a uni directional model of either excitation/inhibition.

Anger and the Brain/The Neuropsychology of Anger

2011-12-20T02:24:00.002-08:00

Often the terms anger and aggression are used interchangeably; however this is somewhat of a faux pas as anger is a feeling and aggression is a behaviour. Central to the neuroanatomy of anger are the amydala, sitting deep with the medial temporal lobes. In cases of anger the amygdala proverbally hijack the prefrontal cortex, driving responses emotionally and impulsively rather than cognitively through reasoning. Biologists have correlated increased testosterone levels with increased amygdala activity.

The hypothalamus is also very important in a neuropsychological understanding of anger. So called 'sham' rage has been manufactured in animal studies where lesions have been introduced to the hypothalamus. More specific animal lesion studies have revealed lateral stimulation results anger with attack responses (Flynn, 1967). Obviousely, ethical criticisms are not the only limitations to these sort of studies as generalisability to humans is at best speculative.

The anterior cingulate cortex, in rather crude terms lies neatly between the affective and cognitive divisions of the brain. More animal experiments have implicated this area of the brain in anger emotional process (Kordidze and Oniani, 1972). But again one has to question whether we can measure the emotions of animals or are we at best merely studying behaviour?

Dougherty et al. (1999) has studied human anterior cingulate cortex activation through inducting anger through narrative scripts and measuring blood flow using PET techniques. Poor scanner accuraacy and high expense limits the value of these types of PET studies, however Denson et al. (2009) used fMRI to reaffirm PET evidence.

The orbito frontal cortex is implicated in impulse control. Bechara et al (1994) carried out lesion studies and ran gambling tasks. The researchers witnessed reckless behaviour in orbito frontal cortex lesion patients. Blair et al (1999) and his high profile psychopathy studies found increased orbito frontal cortex activation for angry faces but not sad or neutral.

The ventromedial cortex activation in anger has also been demonstrated through PET studies Dougherty et al. (2004) CT evidence (Grafmann et al. 1996) and fMRI studies (Lotze et al. 2007).

Kalbe et al. (2004) studied the dorsolateral prefrontal cortex and its role in anger. The researchers found when the dorsolateral prefrontal cortex was active the orbito frontal cortex is inhibited further inhibiting its affective cue processing. Alternatively, when its inhibited the OFC is active and aggressive behaviour is likely to be carried out.

In conclusion, although we now understand which areas of the brain appear to be involved in anger processing, nearly all research relies upon anger induction, often asking people to relive memories. Can we equate this with emotion or is it more similar to a cognition or a cognitised emotionally rich memory?

Personal injury psychological assessment

2011-12-12T14:49:00.000-08:00

For personal injury psychological assessment in the South West of England email: psychologyassessment@yahoo.co.uk or visit www.psychologyassessmentdevon.co.uk

Adjustment and Coping in Acquired Brain Injury

2011-12-12T12:35:00.000-08:00

"People want something to do, somewhere to live and someone to love" (McColl et al. 1998).

Approximately 50% of people who acquire a brain injury will go on to develop chronic anxiety and/or depression (Anson & Ponsford, 2006). Thus there has been a focus on understanding this process in order to help. However, adjustment is a complex process. For a start Impairment does not linearly equate to disability, because disability has a social context, hence it is socially constructed (see Johnston, 1996). Therefore, the process of adjustment to brain injury is mitigated by internal and external, controllable and uncontrollable cognitive, emotional, social, and psychological factors.

The literature on adjustment diverts down many lines of enquiry. There is of course the founding theories of Kubler-Ross (1969) on the stages of grief. This model has undergone many updates moving away from a linear stage model of grief to an acceptance model describing the common feelings of loss in a wider context. This model has great therapeutic use in brain injury, but it still lacks the specificity in predicting positive adjustment and coping.

Of course brain injury carries with it an increased liklihood of specific cognitive factors that may affect coping. For example, reduced problem solving ability, mood dysregulation, lability, memory difficulties, reduced concentration and so on. However, researchers now believe the impact of this is less obvious than one might assume. For instance, although these cognitive dysfunctions are more prevalent in severe brain injuries, adjustment appears to be inversely correlated to severity self awareness and insight is not always a good thing (see Brown & Vandergoot, 1998 'quality of life' studies).

Poor adjustment has often been associated with self-blame, excessive worry, ruminative thoughts, wishful thinking, misuse of drugs and alcohol and general avoidance (Anson & Ponsford, 2006). In addition there appears to be a significant gender divide with females more likely to seek systemic support and males more likely to cope in isolation.

McColl et al. (1998) puts it simply: happier brain injury survivors want 'something to do, somewhere to live and someone to love'. In recent years reserachers have managed to specify positive predictors of adjustment. Some of these include:

-a problem solving approach
-low expectation of outcome and realistic hopes & goals
-internal locus of control
-healthy levels of self esteem
-Use of humour
-personal resilience
-high premorbid intelligence
-supportive families/home environments

I Feel what you Feel

2011-12-11T01:39:00.000-08:00

The Functional Anatomy of Empathy

The main difficulty in understanding emapthy from a neuropsychological perspective is that it is a rather wooley concept, incorporating behaviours and cognitions, metacognitions and emotions. Essentially psychologists will define empathy as the ability for animals to recognise and act accordingly to the emotional state and perspective of others. The following summary of involved brain structures is, out of necessity, unfortunately bastardised. The amygdala is the most obvious place to start. The amygdala is located deep within the medial temporal lobes. It is in close proximity to limbic structures dealing with emotional related matters. Abnormality in the amygdala has been found in a number of clinical presentations, including autism, psychopathy, bipolar disorder and other mood disorders. Functionally the amygdala is involved in emotional learning, embuing memories with emotional significance and moderating their consolidation. It is also thought that it is involved in mitigating social distance and possibly important in sexual orientation (although this is obviously a sensitively politic). Patient SM had extensive damage to the amygdala in each hemisphere. She had no motor, sensory, or cognitive deficits but when asked to identify photographs of a series of facial expressions, SM could identify every expression but one, she could not recognize fear. Similarly, when asked to draw facial expressions, SM produced accomplished pictures of each emotion, but she could not reproduce the expression of fear. When asked about her drawings, she explained that 'she did not know what an afraid face would look like.'

Functional magnetic resonance imaging (fMRI) has been incredibly useful in our understanding of empathy. Recent studies have shown that observing another person's emotional state activates parts of the neuronal network involved in processing that same state in oneself, whether it is disgust, touch, or pain. Almost by accident, researchers Preston and Frans de Waal discovered that monkey's sensory cortices would fire whilst researchers were moving experimental stimuli. So called 'mirror neurons' are neurons that fire both when the creature watches another perform an action as well as when they themselves perform it. In their paper, they argued that attended perception of the object's state automatically activates neural representations, and that this activation automatically primes or generates the associated autonomic and somatic responses, unless inhibited. This mechanism is similar to the common coding theory between perception and action.

Autism often provides a 'case in point' for empathy dysfunction. Anatomically the autistic brain undergoes a statistically significant dvelopmentally governed overgrowth of white matter, with an impeded pruning process, leading to a relative underdevelopmental of grey matter in the frontal lobes especially. Frontal lobe function is incredibly important in attending to and intellectualising the emotional and cognitive states of others. It works in tandom with the aymygdala, the orbito frontal cortex, the medial cortex, the dorsolateral frontal cortex and the frontal gyrus.

The BPS Advised Neuropsychological Assessment Structure

2011-12-11T00:42:00.000-08:00

As part of the process of QICN registration the BPS advise upon a structure for short case studies. It is perhaps a good idea in neuropsychology to practice this structure during assessment. The following titles are advised:

Reason for referral
Background
Brief rationale for Test Selection
Patients Behaviour during the Assessment
Assessment Results and Interpretation
Summary of Results
Recommendations
Appendices

For more information see:
http://exams.bps.org.uk/document-download-area/document-download$.cfm?file_uuid=0E8B11FE-B9C7-959C-E9C4-2B432CE6A7D9&ext=pdf

The neuroanatomy of memory function in the brain

2011-12-10T15:48:00.000-08:00

Much of the brain is involved in memory. Key areas are implicated but realistically these areas are reciprocally integrated in complex ways. But in an attempt to summarise, there are six main areas with more detailed divisions within these areas and new areas implicated by ongoing research all the time. The six areas are:

Prefrontal cortex- this areas is thought to be synonmous with working memory and acts as an attentional device for focusing on things to remember. Often memory recall problems are better conceptualised as attential deficits.

The hippocampus- this area of the limbic system is fundamentally synonymous with long term memory and its consolidation. This area is often affected in subcortial dementias. The landmark case on hippocampus lesion was the case of H.M., who displayed chronic amnesia relating to long term memory consolidation.

The medial temporal lobe is often adversly affected in temporal lobe epilepsy and its treatment sits behind the left ear, and is unsurprisingly related to verbal memory.

The amygdala is ancient in the evolutionary development of the human brain. It is involved in linking important powerful emotions to memory. Its dysfunction has been identified in psychopathy, autism and in PTSD.

The striatum is part of the basal ganglia and is involved in skill acquisition related memories.

The entorhinal cortex is thought to be involved in spatial memory process.

Motor functions of the brain in a nutshell.

2011-12-10T15:20:00.000-08:00

How does the brain control and execute movement? A rather crude summary of motor function would first describe the prefrontal cortex area of the brain as key to planning movement. Moving onward through the brain the premotor cortex prepares and organises the movement. The basal ganglia selects the appropriate movement, the cerebellum coordinates the timing of the movement and finally the primary motor cortex recruits the muscles to execute the movement.

http://www.google.co.uk/search?q=image+of+motor+brain+areas&hl=en&client=safari&tbo=u&tbm=isch&source=univ&sa=X&ei=qOnjTo3TBsHg8gOo8NGYBA&ved=0CDQQsAQ&biw=1024&bih=690

WWW.psychologyassessmentdevon.co.uk

2011-09-18T00:35:00.000-07:00

WWW.psychologyassessmentdevon.co.uk

Based in Devon, UK 'Psychology Assessment in Devon' is a medico-legal psychology assessment service designed to provide expert witness assessment reports for instructing solicitors. All types of psychological assessment can be provided. Including cases involving: neuropsychological assessment of brain injury, psychological impact of injury including PTSD and depression, IQ/learning disability and criminal competence, depression and other mental illness and Disability Discrimination in the work place.

Contact psychologyassessment@yahoo.co.uk to make an enquiry.

Brain injury assessment

2011-05-23T10:47:00.000-07:00

For all types of private brain injury psychological assessment email psychologyassessment@yahoo.co.uk

Traumatic brain injury link

2011-05-14T07:38:00.000-07:00

http://www.traumaticbraininjury.com/

Assessing and defining mental disability under the disability discrimination act

2011-02-15T05:50:00.001-08:00

Psychologists are sometimes instructed to assess a client's mental status for legal disputes involving the Disability Discrimination and Equality Act 2010.

Guidance to the DDA: http://www.equalityhumanrights.com/uploaded_files/guidance_on_matters_to_be_taken_into_account_in_determining_questions_relating_to_the_definition_of_disability.pdf

Assessment of Capacity

2011-02-15T05:31:00.000-08:00

There are five important things to think about when conducting an assessment of capacity:

1. Start off by thinking that everyone can make their own decisions.
2. Give a person the support he/she needs to make decisions before concluding that he/she cannot make his/her own decisions.
3. Nobody should be stopped from making a decision just because others may think it is unwise or eccentric.
4. Anything done for, or on behalf of, a person without capacity must be in his/her “best interests” - a decision which is arrived at by working through a checklist.
5. When anything is done or decided for a person without capacity, it must be the least restrictive of his/her basic rights and freedoms.

Malingering and the Expert Witness Psychologist (Devon/South West)

2011-02-03T03:09:00.000-08:00

An overriding issue in psychology within a medico-legal arena is the issue of malingering. Malingering involves the exaggeration (fake bad) or underplay (fake good) of symptoms, either consciousely or unconsciousely for secondary gain (an ulterior motive). It differs from a number of other presentations, including somatization, health anxiety/hypocondriasis, and medically unexplained symptoms to name but a few. Psychologists should always bare the possibility of malingering in mind, especially during litigation because of monetary gains. The symptoms most commonly feigned include those associated with mild head injury, fibromyalgia, chronic fatigue syndrome, and chronic pain. Failure to detect actual cases of malingering imposes a substantial economic burden on the health care system, and false attribution of malingering imposes a substantial burden of suffering on a significant proportion of the patient population.
Diagnosis and detection

The DSM-IV-TR states that malingering is suspected if any combination of the following are observed:

1. Medicolegal context of presentation
2. Marked discrepancy between the person’s claimed stress of disability and the objective findings
3. Lack of cooperation during the diagnostic evaluation and in complying with prescribed treatment regimen
4. The presence of Antisocial Personality Disorder
However, these criteria have been found to be of little use in actually identifying individuals who are malingering.
Detection
Some features at presentation which are unusual in genuine cases include:
1. Dramatic or atypical presentation
2. Vague and inconsistent details, although possibly plausible on the surface
3. Long medical record with multiple admissions at various hospitals in different cities
4. Knowledge of textbook descriptions of illness
5. Admission circumstances that do not conform to an identifiable medical or mental disorder
6. An unusual grasp of medical terminology
7. Employment in a medically related field
8. Pseudologia fantastica (i.e., patients' uncontrollable lying characterized by the fantastic description of false events in their lives)
9. Presentation in the emergency department during times when obtaining old medical records is hampered or when experienced staff are less likely to be present (e.g., holidays, late Friday afternoons)
10. A patient who has few visitors despite giving a history of holding an important or prestigious job or a history that casts the patient in a heroic role
11. Acceptance, with equanimity, of the discomfort and risk of diagnostic procedures
12. Acceptance, with equanimity, of the discomfort and risk of surgery
13. Substance abuse, especially of prescribed analgesics and sedatives
14. Symptoms or behaviors only present when the patient knows he is being observed
15. Controlling, hostile, angry, disruptive, or attention-seeking behavior during hospitalization
16. Reporting of wild psychological symptoms, and silly wrong answers on questionaires, not likely in patients with similar but real conditions.
17. Fluctuating clinical course, including rapid development of complications or a new pathology if the initial workup findings prove negative
18. Coinciding indigence or homelessness of the patient, with impending cold weather and a need for indoor lodgings.
19. Giving approximate answers to questions, usually occurring in factitious disorder with predominantly psychological signs and symptoms (see Ganser Syndrome)
20. Eagerly endorsing symptoms suggested by a clinician, but not mentioned by the patient, though they would have been prominent and obvious had they been real.
21. A test for factitious mental disorders presents symptoms which are extremely improbable. Endorsing these symptoms which almost never occur can raise doubt of the person's sincerity.

If a psychologist suspects malingering in a case of possible brain damage (i.e. caused by head trauma or stroke), they may look for a discrepancy between the patient's reported functions of daily living and their performance on neuropsychological tests. In theory, any neuropsychological test could be used in this way, depending on the context. No one test, administered by itself, can proffer a diagnosis of malingering, so a neuropsychological examination typically consists of a battery of tests. Two tests commonly used to determine malingering are:
• Minnesota Multiphasic Personality Inventory (MMPI) (see Validity scales)
• The Test of Memory Malingering (TOMM)
The psychiatrist or neuropsychologist may use these tests, and use the DSM-IV TR criteria while adding a "dimensional analysis" to assist in diagnosis and treatment. Dimensional analysis consists of learning the patient’s history, information about similar cases, and the context of the illness, which could help differentiate cases of malingering from factitious disorders. Tests are rarely conclusive but often need to be triangulated and weighed against other forms of information, including presentation and self reported symtpoms as mentioned before.

Private Neuropsychology Assessment in Devon, Somerset and Cornwall (South West)

2011-01-24T03:24:00.001-08:00

Private Neuropsychology Assessment

Private neuropsychological assessment shares many similarities to the work done within the NHS. Private work is often conducted by an experienced psychologist to provide an expert assessment and report that outlines the nature and extent of any genuine cognitive impairment following a neurological event/insult. Often this is in cases of personal injury, but sometimes clinical negligence. Neurological events most relevant to legal work include various types of brain injury (severe/moderate/mild/open/closed/anoxic/diffuse/focal). In recent years post concussion syndrome has caused much debate within neuropsychology and related arenas, as to its validity and suitability for assessment and diagnosis. As the quality of assessments increases through time and experience, the professional concensus is one of better understanding and clearer identification of this syndrome.

More time is spent in private work assessing possible malingering, exaggeration or falsification of symptoms. Treatments are usually recommended following an assessment and report, but are usually carried out by another practioner. Individual psychologists or psychologist consortiums offer private services. Most of these psychologists will work within the NHS and conduct private work part-time or in their spare time. The South West, including Devon, Cornwall and Somerset is a huge geographical area with a restricted number of suitable psychologists available to conduct private neuropsychological assessments.

Demystifying Psychology in Neuro-Rehabilitation: Emotional Support

2011-01-11T02:28:00.000-08:00

The following is a presentation to neuro-rehabilitation multi-disciplinary staff explaining the role of the clinical psychologist when supporting patients with emotional distress.

The Core Roles of a Clinical Psychologist
To work as part of the MDT
To conduct cognitive assessments and to make recommendations
To provide emotional support and psychological treatments to patients who require them…. This is the focus of this presentation.

Common Emotional Symptoms in Neuro-Rehabilitation
Anxiety
Panic
Depression and low mood
Low mood
Trauma
Stress

The Need for Addressing Emotional Symptoms
Primary reason is to address the ongoing personal distress of the patient.
However, emotional symptoms are also addressed because they are:
To the detriment of the rehab potential
Have a negative impact upon family and friends
Increase the risk of suicide/harm

What does emotional support really mean?
Different from full-on therapy
Patient needs to be onboard
Timing has to be right
Sometimes the goals is an improvement in mood, sometimes it preserves mood and ‘gets people through’ a difficult spell.

Other Key Factors of the Patient
Personal history
Personality before the event
Style that they were parented in/early experiences
Psychiatric history (previous mental illness)
Relevance of any neurological deficits
Triggers
Level of support from others
Level of personal resilience and coping style
Interests

A Psychologist Basic Tools: Listening Skills
To provide a safe/private place to talk
To clarify what they mean and to summarise
To listen and resist offering too much opinion or direction
To consider that some behaviours may be ‘attempted solutions’ to a problem
To guide the patient in discovering their own solutions

More Advanced Psychological Techniques
Formulation
Behavioural Experiments
Challenging negative thoughts
Relaxation
Identity work
Stress management
Assertiveness work
Empty chair work
Therapeutic letters

Exercise and Mental Health: An Overview

2010-07-13T05:24:00.000-07:00

The following is presentation of an overview of exercise in mental health which I recently gave. Although not specifically, neuropsychologically based nor neuro-rehab specific, some of the content is relevant in working therapeutically within neuro-rehab settings.

Intro to Sedentary Lifestyles

 Society has become increase sedentary

 Work, travel, domestic, leisure activities

 Urbanisation

 Labour saving devices

 Changes to childhood

 All creating a diversion from the physical role we evolved to do

Footnote:

Exercise is the purposeful application of physical activity

Both concepts have application to the promotion of mental health and wellbeing and both have been researched

Plan for Presentation

So….

 We know generally we don’t get enough

 But we know its society’s fault!!

 We know its generally good for us

But…

 What are the mechanisms/how does it work?

 What are the specific psychological effects?

 How effective exactly is it?

 What about exercise and mental illness specifically?

 How much do we need for an effect?

 What are the current exercise dose recommendations?

 What should we do with exercise as clinicians?

Mechanisms

Bio

Serotonin (Barchas & Friedman, 1963)

Endorphine/opioid system (Harber & Sutton, 1984).

Blood circulation/Cerebral blood flow (Dishman, 1995; Martinsen, 1987).

Realignment of circadian rhythm/sleep (Buxton et al., 2003; Youngstedt, 2005)

Psycho

Anxiolytic and mood enhancing qualities (see latter slides)

Accumulative mood improvements (Baekeland, 1970; Conboy, 1994; Mondin et al., 1996)

Increased tolerance to stress (Salmon, 2001)

Increase in self-esteem (Folkins & Sime, 1981; Fox, 2000)

Flow (Csikszentmihaly, 1990)

Distraction (Daley, 2002)

Control of negative thoughts (Morgan, 1985; 1987)

Improved retrieval of positive thoughts (Clark et al., 1983)

Positive rumination (Feldman et al., 2006)

Skill mastery (Lepore, 1997; Mynors-Wallis et al., 2000)

Spiritual/developmental theories

Social

Behavioural Activation/engagement (Jacobsen et al., 1996)

Socialisation (NHS, 2001; Priest, 2007)

Social inclusion (Taylor et al. 1999; DHSE, 1999)

Value of the group more than its constituent parts?

Drug and alcohol avoidance?

The Key Psychological Effects of Exercise:

Anxiolytic Effects

 Low to moderate anxiety reducing effect (Long & van Stavel, 1995; McDonald & Hogdon, 1991; Petruzzello et al., 1991).

 Exercise has an immediate anxiety reducing effect

 Exercise training has been linked to trait measured reductions anxiety

 Exercise sessions can reduce physiological reactivity and enhance recovery from psychosocial stressors

 Main mechanism: it is believed that accumulative experiences of exercise protect people against physiological and cognitive stress and anxiety by reducing sympathoadrenal or pituitary-adrenal responses. Put another way, exercise presents an opportunity to habituate to similar symptoms to that of anxiety (Mills & Ward, 1986).

Antidepressant Effects

 There is large scale, controlled, cross sectional support for a causal link between exercise and decreased depression (Steptoe and Butler, 1997 and Stephens, 1988)

 Meta-analyses have estimated that Beck Depression Inventory (BDI) Scores decrease by between 0.3 and 1.3 of a standard deviation after exercise by controlled comparison (Craft & Landers, 1998; McDonald & Hogden, 1991; North et al., 1990; Lawlor & Hopker, 2001).

 RCT studies have suggested that physical activity can be as successful at treating depression as psychotherapy or medication for mild and moderate levels (Klein, 1985; Mental Health Foundation, 2004; NICE, 2003).

 Potential for treating comorbid depression (HIV, Dementia, CHF, cancer survivors, forensic)

Self-esteem

 Exercise can promote physical self-worth and body image for males and females

 The effect is strongest amongst children and middle-aged adults, and those with lowest self-esteem

 Support for aerobic and resistance (latter acting quicker) (Fox, 2000)

Cognitive Function

 Majority of cross sectional studies show that fit older adults display better cognitive task performance than less fit adults

 Particularly in attention demanding and rapid tasks

 Small improvement in cognitive functioning of older adults who experience improvement in fitness (Boutcher, 2000)

 Slight beneficial & protective (Broe et al. 1990) effect in AD and other dementias but not VaD (Laurin et al. 2005)

 Anecdotal evidence from physical training focus within non-physical sports (darts, snooker, golf)

Mental Illness

 Inconsistent and poorly controlled evidence (Faulkner, 2005)

 Significant impact upon negative symptoms

 Mixed findings with positive symptoms (Helmsey, 1995)

 Potential risks (esp. in mania (Moore 2010), eating disorders (Szasbo 2000) and poly-medication treated patients (Faulkner 2005

Exercise Routine

 Exercise dependence is extremely rare

 Mixed evidence to who benefits most: sedentary individuals with greater potential (Fasting & Gronningsaeter, 1986; Roth & Holmes, 1987; Simons & Birkimer, 1988; Williams & Lord, 1997) or more regular exercisers who value it higher (Steptoe et al. 1997)

 Some evidence has shown that interruption of exercise routine in athletes/seasoned exercisers can lead to physical symptoms, including somatic anxiety and feelings of inability to cope (Loumidis & Wells, 1998).

 Theories of stress may help explain this (Salmon, 2001 Gauvin & Szabo, 1992; Morris et al., 1990)

Single Dose Immediate Effect

 15 minutes is enough to instigate an increase in positive mood, activation and valence, along with an energising effect whilst walking and a calming effect whilst recovering after walking (Ekkekakis et al., 1999; Ekkekakis & Petruzello, 1999; Thayer, 1987).

 Approx. 65% of MHR but inter-individual difference in preference of intensity (Ekkekakis et al., 2005; Rocheleau et al., 2004).

 Salmon (2001) suggests one way exercise may improve mood is that each single dose has an accumulative effect, increasing the likelihood of triggering positive cognitive appraisals, behaviours and social interactions.

Exercise Guidance

 Recommendations vary slightly according to different sources but most agree that greatest improvement to anxiety, depression and mood is caused by rhythmic, aerobic exercises, that use large muscle groups, such as walking, jogging, swimming, and cycling, of moderate and low intensity (between 50% and 75% of Vo2 max heart rate), conducted for 15 to 30 minutes and performed a minimum of three times a week in programs of 10-weeks or longer (Guszkowska, 2004; NICE 2003).

 Exercise in this format is safe but initially aversive enough to present a challenge, whilst also remaining controllable and offering a sense of achievement on completion (Salmon, 2001).

Questions for the clinician?

 How to we best get across the message?

 How far do we push the message?

 Is it our role?

 How do we integrate exercise interventions into our therapeutic work?

 How do we ensure longevity to the interventions?

 How do we incorporate exercise into relapse prevention?

 Should we and do we practice what we preach?

The Neuropsychology and Psychiatric Consequences of Anabolic-Androgenic Steroid Abuse (AAS)

2010-06-25T03:17:00.000-07:00

AAS refers to the specific use of steriods to increase protein synthesis within cells, which results in the buildup of cellular tissue (anabolism), especially in muscles. More commmonly it is not athletes who seek this effect but recreational body builders. A number of key events in the evolution of this social concern are documented within Kanayama et al. (2008):

Psychiatric effects

In addition to several detrimental physiological consequences*, evidence points to several significant detrimental psychiatric effects of AAS:

1 Increased likelihood of aggression/violence

2 Increased likelihood of mania

3 Increased likelihood of psychosis and paranoia

4 Increased likelihood of mood disorder and depressive illness

5 AAS dependence

6 Increased progression to other illicit drug use

See http://en.wikipedia.org/wiki/Anabolic_steroid

And

http://www.archido.de/index.php?option=com_docman&task=doc_view&gid=2732

* Increased likelihood of hypertension, elavated cholesterol, heart problems, sexual dysfunction, testicular atrophy and infertility.

Neuropsychological Effects

Unfortunately no controlled studies have looked at long term neuropsychological effects of AAS; and this is partly down to the fact that the phenomena is relatively recent with participants at the very most, only passing into middel age now, and that participants are essentially hard to identify and recruit. However, some research has been conducted with animals into the neurophysiological mechanism of AAS. In an animal study male rats developed a conditioned place preference to testosterone injections into the nucleus accumbens, an effect blocked by dopamine antagonists, which suggests that androgen reinforcement is mediated by the brain. Moreover, testosterone appears to act through the mesolimbic dopamine system, a common substrate for drugs of abuse. Nonetheless, androgen reinforcement is not comparable to that of cocaine, nicotine or heroin. Instead, testosterone resembles other mild reinforcers, such as caffeine, or benzodiazepines. The potential for androgen addiction remains to be determined.

The neuropsychological effects of AAS present an urgent opprtunity for clinical research.

The Mental Capacity Act and the Deprivation of Liberty Safeguards

2010-04-20T02:18:00.000-07:00

Mental capacity is an issue in neuropsychology/neuro-rehabilitation when a clients family and the clinical team providing care and treatment are trying to arrange what is in the best interests of the client, because the client may lack the mental function and capacity to make an informed decision. In 2005 a specific act, The Mental Capacity Act (2005) was created, in order to clear up a number of issues:
1. The assessment of a person's capacity and acts by carers and people working with those who lack capacity
2. The provisions whereby people can plan ahead for a time when they may lack capacity
3. Important safeguards
1 The Act makes it clear that any assessment of a person’s capacity must be ‘decision specific’. This means that:

• The assessment of capacity must be about the particular decision that has to be made at a particular time and is not about a range of decisions
• If someone cannot make complex decisions, this does not mean that he/she cannot make simple decisions
• You cannot decide that someone lacks capacity based upon his/her age, appearance, condition or behaviour
• People who have capacity have the right to make poor judgements/decisions- this is not a basis for lacking capacity.
People lacking capacity will include those with dementia, learning disability, mental health problems, brain damage, toxic confusional state and physical injury or illness. The mental incapacity may be permanent or temporary.

Key Principles

There are five important things to think about:

1. Start off by thinking that everyone can make their own decisions.
2. Give a person the support he/she needs to make decisions before concluding that he/she cannot make his/her own decisions.
3. Nobody should be stopped from making a decision just because others may think it is unwise or eccentric.
4. Anything done for, or on behalf of, a person without capacity must be in his/her “best interests” - a decision which is arrived at by working through a checklist.
5. When anything is done or decided for a person without capacity, it must be the least restrictive of his/her basic rights and freedoms.

What does the Act do?

• It aims to clarify a number of legal uncertainties.
• It reforms and updates the current law where decisions need to be made on behalf of others, incorporating good practice into statute and introducing a process.
• It sets out a single test for assessing capacity which is a ‘decision specific test’ (covering emergency decisions; day to day decisions and significant, but not urgent, decisions – including where there are a series of minor decisions which together become significant).
• It covers a wide range of decisions, on personal welfare (including health care) as well as financial matters and substitute decision-making by attorneys or court appointed ‘deputies’. It also clarifies the position where no such formal process has been adopted.
• It includes new rules to govern research involving people who lack capacity and provides for new independent mental capacity advocates to represent and provide support to such people in relation to certain decisions.
• It provides recourse, where necessary and at the appropriate level, to a court with power to deal with all personal welfare (including health care) and financial decisions on behalf of adults who are lacking capacity.
• It replaces the current Court of Protection with a new Court of Protection which has more comprehensive powers.

What does the act mean?

It puts in place a code of practice to give guidance about the legislation. The code must be followed by those working in a professional capacity (e.g. doctors and social workers).

The Act offers appropriate protection for carers (both family members and unpaid carers), as well as health and social care professionals, to those who act in the reasonable belief that they are doing so in the person’s ‘best interests’ when the principles of the Act are followed.

2. The Act sets out provisions whereby people can plan ahead for a time when they may lack capacity

• Lasting Powers of Attorney (LPA)

the Act allows a person to appoint an Attorney to act on their behalf if they should lose capacity in the future. More information on Lasting Powers of Attorney is available.

• Advance decisions to refuse treatment

the Act makes it possible to make an advance decision to refuse treatment should they lack capacity in the future. The Act sets out clear safeguards for the making and application of advance decisions. Further guidance and explanation of advance decisions can found, in Chapter 9 of the Code of Practice.

3. The Act creates important safeguards

• A new Court of Protection

the new Court will have the power to make declarations about whether someone lacks capacity, make orders, or appoint Deputies to act and make decisions on behalf of someone who lacks capacity. More information on the Court of Protection and Deputies is available.

• A new Public Guardian

the Act creates a new public official called the Public Guardian. The Public Guardian will have several duties under the Act including registering Lasting Power of Attorney's (LPA's) and Deputies. The Public Guardian will be supported in his role by a new office called the Office of the Public Guardian (OPG). More information on the Public Guardian and OPG is available.

• Independent Mental Capacity Advocate (IMCA)

an IMCA is someone appointed to support a person who lacks capacity but has no one to speak for them, such as family or friends. They will only become involved when decisions about serious medical treatment or a change in the person's accommodation where it is provided by the NHS or a local authority. More information on the IMCA's can be found on the Department of Health website.

• Research involving people who lack capacity

the Act sets out clear guidelines for research involving people who lack capacity. The research must be approved by an appropriate body, who will also ensure that the research is safe and relates to the person's condition. They must also ensure that the research would not be as effective if they use people who have mental capacity. More information on research and its regulations can be found on the Department of Health website.

• New criminal offence

the Act introduces 2 new criminal offences of ill treatment and wilful neglect of a person who lacks capacity. A person found

The Mental Capacity Act Deprivation of Liberty Safeguard was introduced to specifically protect the freedom of people who cannot make decisions over their treatment and care because of a lack of mental capacity.

The Mental Capacity Act Deprivation of Liberty Safeguards is a new law, which came into force on 1st April 2009.

The safeguards are in response to the 2004 European Court of Human Rights judgement involving an autistic man who lacked the capacity to consent who was kept at Bournewood Hospital by doctors against the wishes of his carers. The court found that he had been deprived of his liberty unlawfully, and the Department of Health committed to introducing new legislation to close the 'Bournewood gap'.

These safeguards provide protection for a very vulnerable group of people who are cared for in hospitals or in care homes registered under the Care Standards Act 2000, in circumstances that deprive them of their liberty, and who are unable to consent (but who are not detained under the Mental Health Act 1983).

The safeguards are designed to protect the interests of an extremely vulnerable group of service users and to:

• ensure people can be given the care they need in the least restrictive regimes

• prevent arbitrary decisions that deprive vulnerable people of their liberty

• provide safeguards for vulnerable people

• provide them with rights of challenge against unlawful detention

• avoid unnecessary bureaucracy

What is a Deprivation of Liberty?

Deprivation of liberty has no clear definition. Many people in hospitals and care homes may have their liberty restricted but not all will be deprived of their liberty. The following factors need to be considered:

• Whether professionals have complete and effective control over assessment, care, treatment, contacts, movement and residence

• Whether the person will be under constant supervision and control and not free to leave

• Whether restraint is used including sedation

• Whether the person would be prevented from leaving if they attempted to do so

• Whether a request from carers for the person to be discharged into their care is likely to be agreed

• Whether the person can maintain social contacts

• Whether the person has choice about their life within the home or hospital

Who do the Deprivation of Liberty Safeguards apply to?

The safeguards apply to anyone:

• aged 18 and over

• who suffers from a mental disorder or disability of the mind – such as dementia or a profound learning disability

• who lacks the capacity to give informed consent to the arrangements made for their care and / or treatment and

• for whom deprivation of liberty (within the meaning of Article 5 of the ECHR) is considered after an independent assessment to be necessary in their best interests to protect them from harm

What are the authorities' duties under the Safeguards?

Hospitals and Care Homes (these are called Managing Authorities) have a duty to:

• provide care and treatment in ways that do not deprive a person of their liberty, or if this is impossible;

• apply to the Supervisory Body for authorisation of the deprivation of liberty.

The Council and the Primary Care Trust (these are called Supervisory Bodies) have a duty to:

• assess any person for whom the Managing Authorities request a deprivation of liberty;

• authorise a deprivation if it is necessary and in the best interests of a person to whom the Safeguards apply;

• set any necessary conditions to make sure the person's care/treatment meets their needs in their best interests;

• set a timescale for how long a deprivation can last;

• keep records of who is being deprived of their liberty.

What should I do if I feel a person is being deprived of their liberty?

Discuss the issue with the hospital or care home. They may be able to change a person's care or treatment to make sure the person is not being deprived of their liberty, or may be able to explain why a person is not actually deprived of their liberty.

Request that the Supervisory Body reviews the person to see whether they are being deprived of their liberty. This request can be by telephone, fax or email. There are standard letters available to use.

Wernicke’s Aphasia

2010-04-13T06:49:00.001-07:00

Wernicke’s aphasia (AKA fluent aphasia/receptive aphasia) is characterised by inappropriate words and the inability to understand spoken language. Speech is preserved with normal rhythm, but language content is incorrect. This may vary from the insertion of a few incorrect or nonexistent words to a profuse outpouring of jargon. Grammar, syntax, rate, intonation and stress are normal. Substitutions of one word for another (paraphasias, e.g. “telephone” for “television”) are common. Comprehension and repetition are poor.

It is often a result of damage to Wernicke’s area, a left laterised focal area in 97% of people (including the majority of left handers). The major deficit of Wernicke’s aphasia can be understood as an inability synchronising objects and ideas with the words that signify them. Patients who recover from Wernicke’s aphasia report that, while aphasic, they found the speech of others to be unintelligible and, despite being cognizant of that fact that they were speaking, they could neither stop themselves nor understand their own words. Contrast this to Broca’s aphasia which is typified by non-fluent speech lacking in grammer.

An example of Broca’s aphasia:
“I am a sig… no… man… uh…., well,…again.”

(These words were emitted slowly and with great effort. The sounds were not clearly articulated and each syllable was uttered harshly, explosively and in a throaty voice. Moreover, Broca’s aphasia is often accompanied by right hemiparesis).

An example of Wernicke’s aphasia:
“Ive done a lot well, I impose a lot, while, on the other hand, you know what I mean, I have to run around, look it over, ?trebbin? and all that sort of stuff”.”

Types of Agnosias

2010-03-08T06:17:00.000-08:00

Agnosia literally meaning “loss of knowledge” is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream

Alexia
Inability to recognize text.

Alexithymia
Whilst not strictly a form of agnosia, alexithymia may be difficult to distinguish from or co-occur with social-emotional agnosia. Alexithymia is deficiency in understanding, processing, or describing emotions common to around 85% of people on the autism spectrum. Alexithymia is believed to be due to an information processing delay in the combined processing of information in the left and right hemispheres, resulting in poor differentiation between body messages and emotions.

Amusia
Or receptive amusia is agnosia for music. It involves loss of the ability to recognize musical notes, rhythms, and intervals and the inability to experience music as musical.

Anosognosia
This is the inability to gain feedback about one's own condition and can be confused with lack of insight but is caused by problems in the feedback mechanisms in the brain. It is caused by neurological damage and can occur in connection with a range of neurological impairments but is most commonly referred to in cases of paralysis following stroke. Those with Anosognosia with multiple impairments may even be aware of some of their impairments but completely unable to perceive others.

Apperceptive agnosia
Patients are unable to distinguish visual shapes and so have trouble recognizing, copying, or discriminating between different visual stimuli. Unlike patients suffering from associative agnosia, those with apperceptive agnosia are unable to copy images.

Apraxia
Is a form of motor (body) agnosia involving the neurological loss of ability to map out physical actions in order to repeat them in functional activities. It is a form of body-disconnectedness and takes several different forms; Speech-Apraxia in which ability to speak is impaired, Limb-Kinetic Apraxia in which there is a loss of hand or finger dexterity and can extend to the voluntary use of limbs, Ideomotor Apraxia in which the gestures of others can't be easily replicated and can't execute goal-directed movements, Ideational Apraxia in which one can't work out which actions to initiate and struggles to plan and discriminate between potential gestures, Apraxia of Gait in which co-ordination of leg actions is problematic such as kicking a ball, Constructional Apraxia in which a person can't co-ordinate the construction of objects or draw pictures or follow a design, Oculomotor Apraxia in which the ability to control visual tracking is impaired and Buccofacial Apraxia in which skilled use of the lips, mouth and tongue is impaired.

Associative agnosia
Patients can describe visual scenes and classes of objects but still fail to recognize them. They may, for example, know that a fork is something you eat with but may mistake it for a spoon. Patients suffering from associative agnosia are still able to reproduce an image through copying.

Auditory agnosia
With Auditory Agnosia there is difficulty distinguishing environmental and non-verbal auditory cues including difficulty distinguishing speech from non-speech sounds even though hearing is usually normal.

Autotopagnosia
Is associated with the inability to orient parts of the body, and is often caused by a lesion in the parietal part of the posterior thalmic radiations.

Color agnosia
Refers to the inability to recognize a color, while being able to perceive or distinguish it.

Cortical deafness
Refers to people who do not perceive any auditory information but whose hearing is intact.

Finger agnosia
Is the inability to distinguish the fingers on the hand. It is present in lesions of the dominant parietal lobe, and is a component of Gerstmann syndrome.

Form agnosia
Patients perceive only parts of details, not the whole object.

Integrative agnosia
This is where one has the ability to recognize elements of something but yet be unable to integrate these elements together into comprehensible perceptual wholes.

Mirror agnosia
One of the symptoms of Hemispatial neglect. Patients with Hemispatial neglect were placed so that an object was in their neglected visual field but a mirror reflecting that object was visible in their non-neglected field. Patients could not acknowledge the existence of objects in the neglected field and so attempted to reach into the mirror to grasp the object.

Pain agnosia
Also referred to as Analgesia, this is the difficulty perceiving and processing pain; thought to underpin some forms of self injury.

Phonagnosia
Is the inability to recognize familiar voices, even though the hearer can understand the words used.

Prosopagnosia
Also known as faceblindness and facial agnosia: Patients cannot consciously recognize familiar faces, sometimes even including their own. This is often misperceived as an inability to remember names.

Semantic agnosia
Those with this form of agnosia are effectively 'object blind' until they use non-visual sensory systems to recognise the object. For example, feeling, tapping, smelling, rocking or flicking the object, may trigger realisation of its semantics (meaning).

Simultanagnosia
Patients can recognize objects or details in their visual field, but only one at a time. They cannot make out the scene they belong to or make out a whole image out of the details. They literally "cannot see the forest for the trees." Simultanagnosia is a common symptom of Balint's syndrome.

Social emotional agnosia
Sometimes referred to as Expressive Agnosia, this is a form of agnosia in which the person is unable to perceive facial expression, body language and intonation, rendering them unable to non-verbally perceive people's emotions and limiting that aspect of social interaction.

Somatosensory agnosia
Or Astereognosia] is connected to tactile sense - that is, touch. Patient finds it difficult to recognize objects by touch based on its texture, size and weight. However, they may be able to describe it verbally or recognize same kind of objects from pictures or draw pictures of them. Thought to be connected to lesions or damage in somatosensory cortex.

Tactile agnosia
Impaired ability to recognize or identify objects by touch alone.

Time agnosia
Is the loss of comprehension of the succession and duration of events.

Topographical agnosia
This is a form of visual agnosia in which a person cannot rely on visual cues to guide them directionally due to the inability to recognise objects. Nevertheless, they may still have an excellent capacity to describe the visual layout of the same place

Verbal auditory agnosia
This presents as a form of meaning 'deafness' in which hearing is intact but there is significant difficulty recognising spoken words as semantically meaningful.[19]

Visual agnosia
Is associated with lesions of the left occipital lobe and temporal lobes. Many types of visual agnosia involve the inability to recognize objects.

Visual verbal agnosia
Difficulty comprehending the meaning of written words. The capacity to read is usually intact but comprehension is impaired.]

The Neuropsychology of ‘Brain Training’ and Cognitive Reserve

2010-03-08T03:45:00.001-08:00

Many 'brain exercise' products have been marketed in recent years, promising to help people stay mentally fit as they age, and even help prevent dementia. However, a systematic review by Pap, Walsh and Snyder (2009) found no good evidence that brain training will either prevent or slow down mental deterioration in healthy older adults.

Mild memory problems are part and parcel of getting older, but more moderate and severe memory problems and cognitive dysfunction are often indicative of a dementia. Alzheimer's disease is the most common type of dementia, followed by vascular dementia. We know that unhealthy lifestyles including smoking, drinking and unbalanced high fat diets can increase our risk. We also know that genes play a role, and that neuro-traumatic events such as strokes or head injury can increase the risk of developing dementia. But many people wonder what they can do to lower their risk.

Pap, Walsh and Snyder (2009) found 10 good-quality studies that looked at cognitive training in healthy elderly people. When they pooled the studies' results, they found that training led to small improvements in specific tasks related to the training. However, they found no evidence that this prevented or slowed the onset of dementia. That's not to say that brain exercises don't have the potential to help, but researchers say that better-designed studies are needed to find out. Part of the problem with the studies so far is that they didn't assess people for very long. So they couldn't say what long-term effects the training might have had on people's risk of dementia. The studies also mainly looked at how well people performed tasks that were closely tied to their training and nothing else. To meaningfully explore the connection between brain training and dementia, studies would need to look at overall brain function as well as people's performance on tasks in everyday life.

Bold claims made by commercial computer games should be interpreted with an element of cynicism until better research is conducted. Scientists do know however, that there is clear evidence that physical exercise and a balanced diet can delay the progress of dementia significantly. Although the preventative effects of both of these factors is thought to be modest.

Cognitive reserve is valuable way of conceptualising one’s vulnerability to dementia and prognosis. The term cognitive reserve describes the mind's resilience to neuropathological damage of the brain. In the first study of its kind in Katzman et al. published findings from post-mortem examinations on 137 elderly persons unexpectedly revealed that there was a discrepancy between the degree of Alzheimer’s disease neuropathology and the clinical manifestations of the disease. This is to say that some participants whose brains had extensive Alzheimer’s disease pathology, clinically had no or very little manifestations of the disease. Furthermore, the study showed that these persons had higher brain weights and greater number of neurons as compared to age-matched controls. The investigators speculated with two possible explanations for this phenomenon: these people may have had incipient Alzheimer's disease but somehow avoided the loss of large numbers of neurons, or alternatively, started with larger brains and more neurons and thus might be said to have had a greater ‘reserve’. This is the first time this term is used in the literature in this context.

The study sparked off interest in this area and to try to confirm these initial findings further studies were done. Higher reserve was found to provide a greater threshold before clinical deficit appears. Neuronoal density rather than brain size appear to be significant in high cognitive reserve individuals. Moreover, genetics again appear to play a part. Childhood cognition, educational attainment, and adult occupation all contribute to cognitive reserve independently. The strongest association in this study was found with childhood cognition. However, cognitive reserve is somewhat of a double edged sword, as it is believed that people with high reserve go undiagnosed until neuronal damage is severe, then rapid decline ensues.

Reference
Pap KV, Walsh SJ, Snyder PJ. Immediate and delayed effects of cognitive interventions in healthy elderly: A review of current literature and future directions. Alzheimer's & Dementia. 2009; 5: 50-60.

http://en.wikipedia.org/wiki/Cognitive_reserve

The Neuropsychology of Loss

2010-03-04T08:19:00.000-08:00

Loss is a key process in adjustment to and acceptance of one's limitations following a neurological event such as a brain injury, stroke or neurological disorder. Loss refers to any concept of value that has been detrimented following a neurological event.

Common losses include: Independence; Mobility; Relationships; Ability to communicate; Career/Job; Friends; Memories; Self-awareness; Hobbies & interests; Driving; Freedom; Sex/sexual drive; Routine; Prospects etc.

Psychotherapists have often discussed the stages of loss that people tend to experience. However, these stages are not regularly experienced in a serial or linear fashion and therefore more recently psychotherapists and psychologists tend refer to the 'common feelings' of loss rather than the 'stages of loss'.

Although there is little scientific confirmation for the 'common feelings of loss', an overwheling majority of psychotherapists and psychologist agree, from many years clinical experience of providing therapy that there five 'common feelings' that appear to involved in loss.

1 Denial
* We deny that the loss has occurred or ignore the signs.
* We may use fiction or fantasy to deny the reality or make sense of confusing partial memories.
* We may withdraw believing we can avoid facing the loss and avoid those people who confront us with the truth.
* We may regress to being like a child who wants protecting from the loss.

2 Bargaining
* We may promise to do anything to make this loss go away.
* We may bargain or strike a deal with God, ourselves or others to make the loss go away.
* We lack confidence in our attempts to deal with the loss, looking elsewhere for answers or gamble on a miracle.

3 Anger
* Anger is a perfectly natural reaction to loss that passes with time.
* Anger can come from loss, grief, frustration and resentment and we can become angry with:
A Ourselves: ‘self blame’.
B Others: ‘kicking the cat’
C Our closest friends and family

4 Despair
*We become overwhelmed by the anguish, pain, sadness and hurt of our loss
*Our mood can be lowered and we might often cry
*We might wrongly convince ourselves that the loss was some sort or payback.
*We might begin feel despondent and to think things are utterly hopeless.

5 Acceptance
*We can identify losses and the common feelings of loss.
*We can describe the details of our loss and the details of the rehabilitation.
* We can get through each day, cope somehow and keep sight of some level of hope.
* We are now aware when we dip back into stages or common feelings of loss and know what to do to help.
* Adapt and drive toward our potential.

Acceptance presents the final and most adaptive phase of feeling associated with loss. Therapeutic aims are often based upon experiencing more feelings associated with acceptance.

There is a growing collection of evidence that loss has neurological consequences. fMRI scans of women from whom loss and grief was elicited about the death of a mother or a sister in the past 5 years found it produced a local inflammation response as measured by salivary concentrations of pro-inflammatory cytokines. These were correlated with activation in the anterior cingulate cortex and orbitofrontal cortex. These activation also correlated with free recall of grief-related word stimuli. This suggests that grief can cause stress, and that this is linked to the emotional processing parts of the frontal lobe.

Among those bereaved within the last three months, those who report many intrusive thoughts about the deceased show ventral amygdala and rostral anterior cingulate cortex hyperactivity to reminders of their loss. In the case of the amygdala, this links to their sadness intensity. In those who avoid such thoughts, there is a related opposite type of pattern in which there is a decrease in the activation of the dorsal amgydala and the dorsolateral prefrontal cortex.

In those not so emotionally affected by reminders of their loss, fMRI finds the existence of a high functional connectivity between the dorsolateral prefrontal cortex and amygdala activity, suggesting the former regulates activity in the latter. In those who had greater intensity of sadness, there was a low functional connection between the rostal anterior cingulate cortex and amygdala activity, suggesting a lack of regulation of the former part of the brain upon the latter

Working with Challenging Behaviour in Neuro-Rehabilitation

2010-02-17T01:47:00.000-08:00

Dealing with challenging behaviour is much the same in neuro-rehabilitation as it is in other care and therapeutic contexts. The following is the basis of a training workshop in progress aimed at increasing skills in dealing with challenging behaviour wihtin a neuro-rehab setting.

What do we mean by challenging behaviour?
Behaviours are actions that we can observe and record:
Hitting
Kicking
Biting
Spitting
Smearing
Self-harm
Swearing
Disinhibition
Sexualised actions
Verbal threats?
Stubborness?
Lack of insight?

Emerson’s definition
"culturally abnormal behaviour(s) of such intensity, frequency or duration that the physical safety of the person or others is placed in serious jeopardy, or behaviour which is likely to seriously limit or deny access to the use of ordinary community facilities"

How do we learn behaviours?
From reward (reinforcement)
Through association
From role modelling
From unique human ability of reflection on action/learning from mistakes?

How do we unlearn behaviours?
Through punishment?
Through negative reinforcement?
Through extinction?
Through rewarding alternative experiences

Why do challenging behaviours arise?
Behaviours or actions exist because they serve a function
Challenging behaviours are no different
Functions:
Get needs met
Communicate thoughts/feelings
Avoidance
Sensation

Maintaining and promoting rules & boundaries:
Don’t be afraid to say when CB is not appropriate- clearly describe to a client when behaviour unacceptable
Consistency is key
Maintaining equal/professional relationships
Promoting team approaches rather than split teams

Improved communication:
What is the behaviour trying to express?
Functional assessment/ABC analysis
Liaison with speech and language
Communication aids/development
Relationships

Proactive strategies and environmental changes:
Consistency is key: Follow nursing guidelines/plans
Observe and record what rewards apply to an individual
Assessment of Frequency-Intensity-Duration-Onset (FIDO)
Think about environment/places/people/promiximity etc
Make environment safe when addressing CB
Be aware of cognitive limitations when planning activities

Reactive strategies:
Consistency is key: following team nursing guidelines
Make sure people are safe
Firstly, state when behaviour is unacceptable
Secondly, guide toward alternative behaviours
Reward positive alternative behaviours
Team liaison
Try not to inadvertantly reinforce CB
Time out strategies only work if followed to the tee with no exceptions

Awareness of feelings/attributions:
Challenging behaviour can evoke strong feelings in us. Sometimes they create anger/sadness/guilt/dislike. Incidents can sometimes remind us of previous experiences, events or people.
The feelings are really important because:
They can influence how we respond and deal with the behaviour

Talking about CB to colleagues and learning from past events:
CB creates staff stress
Evidence says support/talking helps
Open culture of learning from mistakes
Psychology’s door is open if strong feelings arise

Responding to Challenging Behaviour Summary:
Maintaining and promoting rules & boundaries
Improved communication
Proactive strategies and environmental changes
Reactive strategies
Awareness of feelings/attributions
Talking about CB to colleagues and learning from past events

Accelerated Forgetting and the Neuropsychological Assessment of Memory in Epilepsy

2010-02-09T02:41:00.001-08:00

Patients with epilepsy frequently complain of memory difficulties yet often perform normally on standard neuropsychological tests of memory. It has been suggested that this may be due to an impairment of very long-term memory consolidation processes, beyond those normally assessed in the neuropsychological clinic.

Blake et al. (2000) found despite normal learning and retention over 30 min, patients with epileptic foci in the left temporal lobe performed disproportionately poorly on the long-term test compared with both patients with epileptic foci in the right temporal lobe and controls. Findings provide evidence for an extended period of memory consolidation and point to the critical region for this process, at least for verbal material, in the left temporal lobe.

Zeman et al. 1998 studied the concept of transient epileptic amnesia (TEA). TEA usually begins in later life, with a mean age of 65 years in this series. Episodes are typically brief, lasting less than one hour, and recurrent, with a mean frequency of three a year. Attacks on waking are characteristic. Repetitive questioning occurs commonly during attacks. The anterograde amnesia during episodes is, however, often incomplete so that patients may later be able to “remember not being able to remember”. The extent of the retrograde amnesia during attacks varies from days to years. Most patients experience other seizure types compatible with an origin in the temporal lobes, but transient amnesia is the only manifestation of epilepsy in about one third of patients. Epileptiform abnormalities arising from the temporal lobes are most often detected on interictal sleep EEG. Despite normal performance on tests of anterograde memory, many patients complain of persistent interictal disturbance of autobiographical memory, involving a significant but variable loss of recall for salient personal episodes. He hypothesises that post ictal states (5-30 mintues following seizure) may be responsible for disrupting the consolidation of long term memories, thus explaining accelerated forgetting. Direct links between temporal lobe epilepsy and memory difficulties is complicated by a number of confounding variables:

• Anti-convulsent medication side effects
• Age of epilepsy onset
• Seizure frequency
• Structural damage arising from epileptic activity

See Butler and Zeman for a comprehensive and up to date review of the issues
http://brain.oxfordjournals.org/cgi/reprint/131/9/2243

Improvised Neuropsychological Assessment

2010-02-04T08:36:00.001-08:00

Neuropsychological batteries and tests are usually reliably normed, conceptually well validated and thorough. However, they often take a long time to administer and are sometimes not at hand when assessment opportunities present themselves. Moreover, they are often not practicable or a client develops an adversity to testing.

Informal 'on-the-spot' testing using a magazine on a topic they are interested may provide a 'make shift' or improvised assessment opportunity.

Using Something as accessible and simple as a magazine can provide many assessment opportunities:

Memory- LTM can be assessed by using magazine features to trigger autobiographical memories; new memories can be assessed by asking the client to remember an item in the magazine for testing later; WM can be testing by asking a client to repeat back a short story or sentence.

Neglect- Look for missed words/pictures when asked to read/describe magazine.

Apraxias- Point to items, turn pages, match items in magazine to surroundings.

Praxis- can the client name items/objects in magazine.

Comprehension- understand the gist of article

Attention- can concentrate on magazine without distraction/fatigue.

Speech- any read aloud from magazine.

Colour agnosia- are colours recognised/matched?

Prosopagnosia- Are famous faces easily recognised?

Dyslexia- read part? Understand it?

The Neuropsychology of Korsakoff's syndrome

2010-01-26T08:24:00.001-08:00

Korsakoff's syndrome is a brain disorder caused by the lack of thiamine (vitamin B1) in the brain, often caused by heavy drinking restricting nutritional intake or through physical changes to the stomach lining restricting its ability to absorb thiamine. The syndrome is named after Sergei Korsakoff, the neuropsychiatrist who popularized the theory

Although often referred to as Korsakoff's psychosis or Korsakoff's dementia, in an attempt to describe its similar features to a dementia or to a psychotic episode, it is in fact best described as a syndrome or a ‘collection of symptoms’. This is because following the initial period of confabulatory/’psychotic-like’ features, cognitive functioning and orientation tends to be restored close to premorbid levels.

Physiology

On a physiological heavy levels of prolonged alcohol use (a neuro-toxic) create enduring changes of chemistry with the brain. Deficiency of thiamine along with prolonged neurotoxicity within the brain result in general cerebral and ventrical atrophy, damage to hippocampus, the medial thalamus and possibly to the mammillary bodies of the hypothalamus.

Neuropsychological Symptoms

Cerebral atrophy inherent in Korsakoff's syndrome presents like an accelerated ageing of the brain. Deficits in speed of information processing are most obvious, along with 6 other key features:

1. anterograde amnesia and
2. retrograde amnesia, severe memory loss
3. confabulation, that is, invented memories which are then taken as true due to gaps in memory sometimes associated with blackouts
4. meager content in conversation
5. lack of insight
6. apathy - the patients lose interest in things quickly and generally appear indifferent to change.

Wernicke's encephalopathy refers to the initial symptoms that often preclude Korsakoff’s syndrome (especially when left untreated). Wernicke's encephalopathy includes symptoms of: involuntary or jerky eye movements, paralysis of muscles, poor balance, staggering gait or inability to walk and drowsiness and confusion. Korsakoff’s syndrome is therefore on the more severe end of a spectrum, and sometimes this spectrum is referred to as: Wernicke-Korsakoff syndrome.

Treatment

Thiamine treatment is often successful in initiating the spontaneous phase of recovery. Longer term recovery focuses upon changes in lifestyle to include alcohol abstinence, regular exercise and a balanced diet.

Recovery

Recovery to premorbid levels of functioning has been repeatedly reported following five years of abstinence from alcohol, although may partly be explained by the ageing process ‘catching-up’ to put it crudely.

The neuropsychology of Multiple Sclerosis (MS)

2010-01-25T05:36:00.001-08:00

Multiple Sclerosis

People with Multiple sclerosis (MS) represent a core client group for the work of a Clinical Psychologist working in Neuropsychological rehabilitation. The first blog I’ve chosen to post is centred upon MS.

A Brief Definition

MS is a disease of the central nervous system (CNS) marked by numbness, weakness, loss of muscle coordination, and problems with vision, speech, and bladder control. It is an autoimmune disease in which the body's immune system attacks myelin, a key substance that serves as a nerve insulator and helps in the transmission of nerve signals. The progress, severity and specific symptoms in MS are unpredictable. One never knows when attacks will occur, how long they will last, or how severe they will be. Most people with MS are between the ages of 20 and 40 at the time of diagnosis. The term "multiple" refers to the multiple places in the CNS that are affected and to the multiple relapses and remissions characteristic of MS.
MS causes demyelinization of the white matter of the brain, with this process sometimes extending into the gray matter. Demyelinization is loss of myelin, which is composed of lipids (fats) and protein. The white matter is the part of the brain which contains myelinated nerve fibers and appears white, whereas the gray matter is the cortex of the brain which contains nerve cell bodies and appears gray. When myelin is damaged in MS, nerve fiber conduction is faulty or absent. Impaired bodily functions or altered sensations associated with those demyelinated nerve fibers give rise to the symptoms of MS. Watch this clip on you tube for a quick run down on physiology:

http://www.youtube.com/watch?v=qgySDmRRzxY&feature=youtube_gdata

The understanding of the basic causes of the disease is notably incomplete. It is known that nerve cell death is part of the nervous system injury in MS. It is known, too, that in MS some types of blood cells, namely lymphocytes and monocytes, gain access to the central nervous system by breaking through the blood-brain barrier at sites of inflammation. The migration of these cells across the endothelium (lining of the blood vessels) and the activation of these immune cells depends on the cell surface molecule called integrin.
Ref: http://www.medterms.com/script/main/art.asp?articlekey=4457

Cognitive Deficits associated with MS

From a neuropsychological point of view MS often affects higher order cognitive functioning, typically causing deficits in speed of information processing and memory (cued and visual). In addition deficits in attention, executive function and verbal fluency are often reported and in some cases visuo-spatial problems. Cognitive deficits are one of the main symptoms of MS although they are often mitigated by stress and low mood. Intact abilities often include, rate of learning, liklihood of remembering a specific item based on when it was presented, identifying semantic characteristics of learned material, and incidental learning (learning without the need for significant attention). Recognition of these deficits is relevant both to the diagnosis and rehabilitation of this disorder.

Lazeron et al. (2006) looked at the neuropsychological profile of patients with MS. In the study thirty two patients with MS undertook MRI scans and thorough neuropsychological assessment.
Results indicated a decrease in the speed of processing and response speed stability, and a decrease in psychomotor accuracy and stability were clearly associated with less brain volume, and with higher lesion loads, in particular at frontal and occipital areas. Correlations with brain volume reduction were found for all domains, except for visuo-spatial processing. In particular, speed and speed fluctuation scores correlated with brain volume reduction, while accuracy of performance, in general, did not correlate. Only some test speed scores and speed fluctuation scores correlated with lesion load measurements. This study showed that, in MS patients, accuracy of processing is not compromised unless high working memory demands are involved. Problems in neurocognitive functioning in MS are mainly modulated by speed and stability of speed processing, in particular when attention-demanding controlled information processing is required. Abnormalities in these domains are most strongly associated with brain volume loss, confirming that pathology beyond focal lesions is important in MS.
Ref: http://msj.sagepub.com/cgi/content/abstract/12/6/760

Psychological support for MS

For people with MS the emotional aspects of living with a long-term condition can prove just as challenging as the physical aspects of the condition. MSis a major cause of neurological disability in young adults. There are at least five major factors of psychological adjustment to MS:

1. The personality of the patient
The first factor of psychological adjustment to multiple sclerosis is the personality of the patient. Some patients adapt quickly to new life whereas others are trapped in the stage of disbelief and continue to be depressed for a long time after the diagnosis.

2. The quality of family support
The second factor of psychological adjustment to multiple sclerosis is the quality of support available to the patient within his family. All stakeholders should have an idea about the family dynamics before, during and after diagnosis. They should ask the following questions: Does the patient have a life together? What kind of relationship the patient has with his close relatives (children, spouse, and extended family)? The answers to these questions are important because the psychological suffering of a patient may result from tensions within his family (rejection, stigma, exclusion, indifference). Often a psychological maltreatment develops between the patient and his relatives; they feel unable to bear the daily progress of the disease.

3. The skills of social openness
The skills of social openness are the third factor of psychological adjustment to multiple sclerosis. They in fact correspond to how the patient is able to seek support and mental peace in his surroundings especially his family and friends. It helps the patient feel supported in the unhappy moments. Continuing his or her job helps the patient cope up with the new realities associated with the disease because continuing work lifts up the spirit of the patient and fills him with the feeling of productivity.

4. The quality of the relationship with the health professionals
The quality of the relationship of the patient with the health professionals (in the broadest sense, which also includes paramedical workers also) plays as a factor in psychological adjustment to multiple sclerosis. The patient has a high level of dependence on his doctor for psychological support as well as for the management of the disease.

5. The disease
The disease and its prognosis play an important role in the psychological adjustment of patients with multiple sclerosis. If the disease progresses slowly, the patient gets accustomed to his newly acquired disabilities gradually but if the disease has a rapid progression, the patient can not adjust and his life is compromised both physically and psychologically.

Ref;
http://ezinearticles.com/?The-5-Major-Factors-of-Psychological-Adjustment-to-Multiple-Sclerosis&id=2435238

What can a clinical psychologist contribute to an MS service? Boot et al. (2008) report the results of a team audit.

Figure 1. Psychological Symptoms on Assessment for MS Patients

What support was offered by the clinical psychologist?
The number of sessions offered was agreed between the clinical psychologist and the person with MS. People attended an average of three sessions, on a monthly basis. However, up to fifteen sessions were arranged, depending on individual requirements. A broad range of psychological interventions was provided. For some people, exploring options for change and being given self-help information about low mood, anxiety, falls and relationship difficulties was enough. Psychological therapy was used with people whose difficulties were more complex. Clinical psychologists learn a range of therapeutic approaches during their training. Different approaches were integrated in a way that best fit with the person and the problems they were experiencing. Partners and other family members were included at times so that they could discuss the best way of adjusting to the situation together. When problems with memory and thinking were identified, strategies to support these difficulties were developed. Some support over the telephone in conjunction with self-help information was occasionally provided for people who were unable to travel to the MS clinic.
According to Boot et al. (2008) psychological input can have benefits in the following areas:
• Managing their mood better
• Coping better
• Improved levels of daily activity
• Better understanding of their difficulties
• Improved relationships
• Less prone to feelings of suicide
• More confident about managing their future with MS.

Conclusions
This audit highlights the range and varying complexity of difficulties described by this group of people with MS, who were referred to a clinical psychologist. It shows how a number of different factors in people's lives can contribute to emotional difficulties. A flexible and individualised approach was used to provide psychological interventions that fit with the person and the problems they are experiencing at that time. The process facilitates individual management of emotional difficulties and encourages the individual to seek further support should they feel the need in future. These processes meet the government directives on managing long-term conditions, which promote self-care.

Ref: http://www.mstrust.org.uk/professionals/information/wayahead/articles/12042008_04.jsp

Support: http://www.mssociety.org.uk/

Defining neuropsychology

2010-01-24T14:58:00.000-08:00

Neuropsychology or clinical neuropsychology concerns itself with the evaluation and treatment of functional consequences of neurological (especially cerebral) damage. It is a different way of looking at certain aspects of the brain-behavior relationship that may be helpful to physicians in all specialties. Over the next few posts I'll begin to introduce and discuss the neuropsychology and clinical implictions of various neurological disorders and brain injuries.

Neuropsychology blog begins

2010-01-24T13:16:00.000-08:00