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Clinical Neuropsychology

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Brain can be divided into four lobes: Frontal, Parietal, Occipital, Temporal ... Huntingtons Disease: frontal signs, visual memory deficits, depression. PSP, SRO ... – PowerPoint PPT presentation

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Title: Clinical Neuropsychology


1
Clinical Neuropsychology
  • Aims and Objectives
  • By the end of this lecture you will have learned
  • The most common aims of a clinical
    neuropsychological assessment
  • A brief review of the behavioural geography of
    the brain
  • The types of patient most often seen by clinical
    neuropsychologists (e.g. the types of brain
    damage which typically cause neuropsychological
    deficits)
  • Suggested reading
  • Lezak, M (1995).Neuropsychological assessment.
    CH1, CH7
  • Kolb Whishaw?

2
Aims of Clinical Neuropsychology
  • Determine Pathology / Lesion localisation
  • E.g. are memory deficits in an elderly patient
    due to depression / stroke?
  • Clinical Neuropsychologists can build up picture
    of brain damage sites by testing patient with
    tests known to be sensitive to damage in specific
    brain areas
  • Increasingly redundant now due to the advent of
    neuroimaging techniques
  • But in some cases sophisticated testing can
    indicate damage when imaging techniques show no
    gross damage (e.g. hypoxia, heavy metals,
    psychiatric disorders)

3
Aims of Clinical Neuropsychology
  • 2. Characterise cognitive deficit
  • Clinical neuropsychologists can build an accurate
    picture of patients cognitive strengths /
    weaknesses
  • E.g. How severe are memory impairments? Will they
    impact on everyday life?
  • Has important implications for the development of
    rehabilitative programs.
  • E.g. is info retained if presented visually
    rather than verbally?

4
Aims of Clinical Neuropsychology
  • Determine a baseline performance
  • Clinical neuropsychologists often perform
    comprehensive batteries before and during various
    neurosurgical procedures
  • E.g Excisions for epilepsy, psychosurgery,
    implanting neural stimulators
  • Post-surgery testing allows an assessment as to
    whether functions have improved or deteriorated.

5
Functional Neuroanatomy
Brain can be divided into four lobes Frontal,
Parietal, Occipital, Temporal
6
Functional Neuroanatomy Orientation
  • 3D Structure so described in 3 Dimensions
  • There are lots of different terms used
  • They make more sense for rats
  • Some Latin
  • Rostrum Beak
  • Caudalis Tail
  • Dorsum Back
  • Ventrum Belly
  • Latus Side
  • Medius Middle
  • Other dimension
  • Lateral / Medial
  • Combinations are common - eg. Dorsolateral /
    Ventromedial

7
Functional Neuroanatomy Orientation
  • 3 Dimensions describe 3 perpendicular planes
  • Horizontal (aka Axial or Transverse)
  • e.g. MRI / PET Images
  • Midsagital or parasagittal

8
Neuroanatomy - Frontal Lobes
Can be divided into
  • Motor Control of movement
  • - weakness / paralysis
  • Premotor Integration of motor skills / learned
    action
  • - uncoordinated movements / impaired motor
    skills / speech
  • Prefrontal Complex cognitive functions
  • - difficulties with planning / decision making /
    inhibition / memory / attention / perseveration /
    personality changes / aphasia etc etc.

9
Neuroanatomy - Parietal Lobes
  • Functions
  • Sensory integration, visual attention,
  • Lesions can cause
  • Neglect, extinction, dyscalculia, anomia,
    agraphia, alexia

10
Neuroanatomy - Temporal Lobes
  • Functions
  • Memory, auditory processing, object
    categorisation
  • Lesions can cause
  • Amnesia, Wernickes aphasia, prosopagnosia,
    category specific deficits.

11
Neuroanatomy - Occipital Lobes
  • Functions
  • Sensory integration, visuoperception, vision
  • Lesions can cause
  • Heminopia, Blindsight, Visual Agnosia, Colour
    Agnosia

12
Common Causes of Neuropsychological Deficits
  • Head Injury
  • Penetrating
  • Closed
  • Vascular Disorders
  • Ischemic
  • Heamorrhagic
  • MID
  • Neurodegenerative disorders
  • Cortical dementias
  • Subcortical dementias
  • Misc

13
Head Injury
  • Most common cause of brain damage
  • Modern AE practise ensures an increasing supply
    of patients
  • 500 people a day sustain a head injury leading
    to brain damage
  • Patients predominantly healthy young men
  • Average life expectancy after injury 52 years.
  • Severity of head trauma relates to behavioural
    and neuropsychological outcome
  • Only 15 of people sustaining severe head
    injuries ever return to work.

14
Penetrating Head Injury
  • WW I II provided material for the first large
    neuropsychological group studies
  • Although damage may appear local, spreading
    shockwaves may damage other areas
  • Swelling / bleeding may also effect other areas
  • Generally less severe than closed head injuries
  • Despite some discrete cognitive dysfunction, most
    people can return to work
  • But often produce seizures (epilepsy)

15
Closed Head Injury
  • Damage typically occurs in two stages
  • Primary Injury - impact
  • Secondary Injury - consequent physiological
    processes
  • Primary Injury
  • Coup / contrecoup
  • Deceleration contusions
  • Shearing - axons blood vessels
  • Secondary Injury
  • Heamorrhages
  • Ischemia
  • Edema

16
Closed Head Injury
  • Damage can be local or diffuse, most commonly a
    combination
  • Reduction in cognitive efficiency
  • Severity (based on LOC and PTA)
  • Mild 0-20m LOC, 0-60m PTA attentional deficits,
    verbal retrieval problems, emotional distress
  • Moderate 1-6h LOC, 1-24h PTA wide variety of
    defecits - memory problems common, difficulties
    with ADL.
  • Severe gt 6h LOC gt1d PTA comprehensive
    cognitive and emotional dysfunction. Untestable
    for weeks / months

17
Vascular Disorders
  • Stroke (CVA) a focal neurological disorder of
    abrupt development due to a pathological process
    in blood vessels
  • Nervous tissues cannot survive more than a few
    minutes without glucose and oxygen
  • 66 of strokes are non-fatal.
  • Ischemic or Heamorrhagic (but distinction is not
    clear cut)
  • Tend to be lateralised
  • Silent or lacunar strokes - small lesions in
    deep brain structures

18
Vascular Disorders
  • Ischemic (obstructive) strokes
  • Thrombosis buildup of fatty deposits block blood
    vessels
  • Embolism - fatty deposit from elsewhere carried
    to the brain
  • TIAs - emboli pass on before too much damage is
    caused
  • Heamorrhagic strokes
  • Hypertension - tend to be subcortical
  • Aneurysms - e.g. AACoA
  • AVMs
  • Multi-Infarct Dementia (MID)
  • Repeated small infarctions
  • Often misdiagnosed as DAT

19
Degenerative Disorders
  • Cortical Dementias
  • Alzheimers Disease (DAT). Memory most effected
    in early stages
  • Frontotemporal Dementia (fvFTD, tvFTD) -
    dysexecutive problems, semantic dementia
  • Subcortical Dementias
  • Parkinsons Disease Some frontal signs
  • Huntingtons Disease frontal signs, visual memory
    deficits, depression
  • PSP, SRO
  • Multiple Sclerosis

20
Degenerative Disorders
  • Toxic conditions
  • Alcoholism
  • Korsakoffs Syndrome
  • Recreational Drugs
  • Environmental / Industrial Toxins
  • Solvents
  • Pesticides
  • Metals
  • Infectious Processes
  • Neurosyphilis
  • HIV AIDS Dementia Complex
  • Herpes Simplex temporal / limbic structures most
    affected
  • Tumours
  • Hypoxia
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