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Mish- Scientific Foundations > Focal brain syndromes in neuropsychiatry > Flashcards

Focal brain syndromes in neuropsychiatry Flashcards

1
Q

What does the frontal lobe consist of?

A

Subdivisions of prefrontal cortex
- dorsolateral prefrontal cortex
- orbital prefrontal cortex
- medial prefrontal cortex

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2
Q

What are the psychiatric symptoms associated with the dorsolateral prefrontal cortex?

A

classic dysexecutive function:

  • difficulties with planning, organization, generation of ideas, inflexibility and poor abstraction skills.
  • Impaired ability to organize events in a temporal sequence (right order/time)
  • unconcern for past/future consequences of their actions
  • forced utilisation behavior: reach out and use objects that are presented to them
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3
Q

What neuropsychiatric tests are done for dorsolateral prefrontal cortex lesions?

A

Similarities/differences test

BUT
frontal lobe paradox (normal in cognitive tests but difficulties in real world)

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4
Q

What are the causes of dorsolateral prefrontal cortex lesions?

A

Tumours, cerebrovascular accidents and frontal neurodegeneration

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5
Q

What are the psychiatric symptoms associated with lesions in the orbital prefrontal cortex?

A

Disinhibition, restlessness, impulsiveness, perseveration, aggression, euphoria, imitation, utilization, compulsive behavior, inappropriate social behavior, impaired empathy, impaired theory of mind

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6
Q

What are the physical symptoms of orbital prefrontal cortex lesions?

A

close to bony protrusions; vulnerable to injury from rotational forces (brain bashes against protrusion) = can cause damage

may be diffuse white matter damage undetectable with functional imaging

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7
Q

What are the causes of orbital prefrontal cortex lesions?

A

frontal tumors, multiple sclerosis, frontal neurodegeneration, anterior cerebral artery (CVA)

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8
Q

What are the psychiatric symptoms associated with medial prefrontal cortex?

A

Apathy, loss of initiative, diminished motor activity, general and emotional indifference, reduced social interest, impaired problem solving, loss of engagement with activities of daily living, hyperorality and loss of insight

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9
Q

Bilateral lesions lead to

A

akinetic mutism

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10
Q

What are the causes of medial prefrontal cortex lesions?

A

trauma, hydrocephalus, bilateral anterior cerebral artery occlusion and tumors of thalamus, 3rd ventricle, hypothalamus and pituitary

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11
Q

What clinical tests are used for frontal lobe function determination?

A

Luria’s motor sequencing- perform rapid sequence motor tasks (fist, palm, edge, flat)

Desk tap test- taps table once or twice with rules/changes rules see if can follow

Proverb interpretation e.g. explain “the grass is always greener on the other side”

Similarities/differences- describe between objects

verbal fluency- generate as many words with certain letter

cognitive estimates- estimate response to simple numerical question (how tall is bus)

stroop test- name of color with different color

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12
Q

What are the roles of the parietal lobe?

A

integral to perception of external space and body image (where we are in physical word, where body is, what its doing, movement)

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13
Q

parietal lobe anatomically underlies

A

the parietal bone of the skull

differentiated into dominant (left if right handed) and non dominant (right if right handed)

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14
Q

What are the psychiatric symptoms of non-dominant parietal lesions?

A

disturbed body image and impaired sense of position in external space- particularly for contralateral side

may be a denial of (anosognosia) or indifference (anosodiaphoria) towards the disability

left sided limbs cannot be recognized or entirely disowned (asomatognosia)

dyscalculia may be a feature (bad arithmetic)

neglect of left side of external space can occur

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15
Q

What are the psychiatric symptoms of lesions in the dominant parietal lobe?

A

associated with dysphagia and agonisa

dysphasic patients speak slowly, make grammatical errors and mistakenly labelled as confused or uncooperative

astereoagnosia- patient cannot name (with eyes closed) a familiar object held in hand based on weight and 3D characteristics

agraphesthesia- number/letters written on patients skin not recognized by touch

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16
Q

Distinguish between where primary motor and sensory dysphasias occur?

A

primary motor dysphasia= anterior lesion

primary sensory dysphasia = posterior lesions

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17
Q

which lesion causes visual agnosia

A

posterior lesions (parieto-occipital)

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18
Q

what are the neurological features of parietal lobe lesions?

A

cortical sensory loss, impaired sensory localization, sensory and visual inattention, mild contralateral hemiparesis seen also maybe contralateral homonymouse lower quadrantopia

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19
Q

What clinical tests are used for parietal lobe function?

A

drawing a clock face (usually only draw 1 side)

  • Recognition of familiar object in hand (with eyes
    closed)
  • Reading - if neglect, may ignore the left side of the page
  • Writing
  • Arithmetic
  • Dressing - look for apraxia (issues with buttons, tie, cufflings)
  • Neurological examination
  • Visual field examination - contralateral homonymous
    lower quadrantopia
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20
Q

Temporal lobe divided into

A

lateral and ventromedial

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21
Q

lateral region is

A

neocortex and has multiple cognitive functions.

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22
Q

ventromedial region contains

A

major components of the limbic system; contributes to emotional regulation.

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23
Q

function of temporal lobe is

A
  • (neurosurgical) stimulation of the temporal lobes can elicit complex perceptions, memories and experiences
  • Déjà vu (strong sense of have experienced before)
  • Auditory, gustatory and visual hallucinations (sudden unfamiliarity in familiar place, partial seizure?)
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24
Q

What are the psychiatric symptoms of dominant temporal lobe lesions?

A

language problems

Receptive dysphasia (Wernicke’s aphasia); severe comprehension deficit to spoken
language develops

  • Expressive speech can become hyperfluent with nonsense words.
  • Lesions of the arcuate fasciculus, which connects Wernicke’s area with Broca’s area, leads to a conduction aphasia, in which the patient has difficulty with repetition.
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25
Q

What are the psychiatric symptoms of non- dominant temporal lobe lesions?

A

may be associated with visuospatial probs

  • Impaired learning of non-verbal patterned information such as music or patterns
  • Prosopagnosia may also be present.
  • Receptive aprosody is associated with non-dominant lesions.

Patients cannot
comprehend other’s intonation and may misinterpret non-verbal socialcommunication.

  • May also fail to recognise familiar voices (phonagnosia).
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26
Q

What emotions are seen during temporal lobe seizure?

A
  • fear,
  • anxiety,
  • pleasure,
  • depersonalisation,
  • depression,
  • déjà vu (familiarity) and jamais vu (unfamiliarity).
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27
Q

Where is olfactory cortex located?

A

The olfactory cortex is located in the uncus and parahippocampal gyrus. Uncus is adjacent to medial hippocampus and the site of mesial temporal sclerosis; may
explain association of TLE and olfactory auras.

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28
Q

Symptoms of epileptic seizures and where it affects?

A

Epileptic seizures affecting the posterolateral dominant temporal lobe may lead to aphasia. There may also be auditory, visual and vestibular disturbances.

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29
Q

Features of mesial temporal seizures include

A

typically exhibit an aura, followed by staring. Oral
automatisms are also common.

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30
Q

Seizures affecting the middle and inferior temporal gyri cause

A

complex
hallucinations or aberrant salience attribution to neutral perceptions

(delusion attributed to perception)

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31
Q

Other temporal lobe syndromes include

A

Bilateral hippocampal lesions and Kluver-Bucy syndrome

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32
Q

What are the symptoms of Bilateral hippocampal lesions?

A

temporal lobe syndromes: * Bilateral hippocampal lesions lead to severe amnestic
syndromes. Inability to store and recall new information.
There may be no other cognitive problems whatsoever.

  • Projections from the hippocampus form the fornix, and in
    turn many of these fibres terminate in the septal nuclei and
    mammillary bodies.

Lesions in these structures can also
produce amnesia i.e. Korsakoff’s syndrome.

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33
Q

Symptoms of Kluver-Bucy syndrome are

A

It is characterised by placidity, hypersexuality,
hyperorality, altered sexual behaviour, visual agnosia, hypermetamorphosis (compulsive exploration of environment) and a failure to learn from aversive stimuli.

34
Q

Kluver-Bucy syndrome caused by what lesion?

A

bilateral medial temporal
lobe lesions.

35
Q

What are the causes of temporal lobe syndromes?

A

Alzheimer’s disease, carbon monoxide
poisoning, fronto-temporal dementia, head injury, herpes encephalitis, temporal lobe stroke, temporal lobectomy and
temporal lobe tumour.

36
Q

How does loss of fear occur (anatomically)?

A

due to bilateral destruction of the amygdala;
has role in the assignation of emotional significance to a
current percept.

37
Q

Deeper lesions within the temporal lobe (anatomically) cause

A

contralateral
homonymous upper quadrant field defects, due to damage to
the visual radiation.

  • May also be mild contralateral hemiparesis due to corona
    radiata damage.
38
Q

What are the clinical tests for temporal lobe function?

A

Speech comprehension (test for receptive aphasia and aprosodia)

  • Word / sentence repetition (test for
    conduction aphasia)
  • Writing/Reading ability
  • Memory
  • -verbal; short term recall of address;
    recall of events in news; knowledge of
    prime ministers / presidents
  • -non-verbal: Rey-Osterrieth Complex
    Figure Test (ROCF); the patient first
    copies the complex geometrical figure,
    then 45 minutes later is asked to reproduce the same figure from the
    memory (recall). It is also a test ofvisuospatial ability (parietal lobe).
  • Visual field testing - contralateral
    homonymous upper quadrantopia
39
Q

What (anatomically) distinguishes the occipital lobe from parietal?

A

on the medial
surface by the parieto-occipital sulcus.

40
Q

What is the function of the occipital lobe?

A

Primarily concerned with higher
order visual processing.

  • Process complex information about
    the form, motion, colour and depth
    of perceived objects.
41
Q

What are lesions of occipital lobes associated with? (symptoms)

A

Relatively common lesions- (posterior cortical artery strokes 5%)

primary visual cortex lesions=
visual blind spots
(scotomas) & partial blind spots (amblyopias)

42
Q

Bilateral lesions of occipital cortex lead to

A

Visual agnosia/prosopagnosia
co occurring with autoprosopagnosia, simultanagnosia, oculomotor apraxia, optic apraxia
possibly present with Balint syndrome

43
Q

What is seen with extensive bilateral occipital cortex lesions?

A
  • Cortical blindness

Loss of vision with normal optic fundi and preservation of pupillary light reflexes.

  • Some patients with cortical blindness exhibit ‘blind sight’; they can sense nearby objects or even discriminate facial expressions but cannot see.

Results from an accessory visual pathway involving the superior
colliculus and pulvinar projecting to dorsal visual areas.
* May be associated with denial of visual loss (Anton’s syndrome).

44
Q

Lesions of the dominant occipital lobe lead to

A

agnosia or pure
alexia for written material, colour agnosia and simultagnosia

45
Q

Achromatopsia (loss of colour vision) may result from a lesion at

A

BA19

46
Q

Bilateral occipitoparietal lesions may cause

A

Charcot-Wilbrand
syndrome, characterised by the loss of ability to create any mental visual images (including re-visualization of dream imagery).

47
Q

What is posterior cortical atrophy?

A

is a neurodegenerative syndrome dominated by
deterioration of higher visual function (particularly visuospatial and visuoperceptual abilities)
as the pathology predominantly affects the occipital lobe.

Patients present to optometrists, ophthalmologists or neurologists with non-specific visual
complaints.
* Diagnosis is often missed

48
Q

What is posterior cortical atrophy caused by?

A

Alzheimer’s disease, also dementia with Lewy bodies, corticobasal degeneration or Creutzfeldt-Jakob disease.

49
Q

What other disorders affect the occipital lobe?

A

Trauma, migraine and epilepsy affecting the occipital lobe may cause elemental
hallucinations (such as flashes of light) and distortion of vision.

Visual auras in epilepsy last only seconds, while in migraine they occur up to an hour before
the onset of headache.

  • Complex visual hallucinations occur more commonly with non-dominant hemisphere lesions.
50
Q

Irritation or damage to visual association cortex causes

A

Dysmorphopsias such as axis shifts, micropsia, macropsia and movement artefacts caused by irritation or damage to the visual association cortex.

51
Q

What is polyopsia and palinopsia?

A

Polyopsia (visual perseveration precipitated by movement/; visual perception of multiple images even after removal of an object from the visual field.)

or after images (palinopsia The appearance of many of the same images while watching a single object is called palinopsia) may
be apparent.

52
Q

What are occipital lobe function tests?

A
  • Visual field testing including detection of
    object movement
  • Naming of familiar objects, colours
  • Reading ability
  • Interpretation and description ‘overall
    meaning’ of a complex visual image (test for
    simultagnosia)- describe whats going on in image
53
Q

What can complete callosal damage lead to?

A

left ideomotor apraxia, right or bilateral
constructional apraxia, left agraphia, alexia in the left visual field and
astereognosis in the left hand. Mutism may also occur.

54
Q

after callosectomy there is often

A

left sided neglect; suggested
to be a result of underactivation of the non-dominant hemisphere.

55
Q

lesions of anterior corpus callosum lead to (symptom)

A

alien hand sign, with
loss of control over the non-dominant hand.

56
Q

Lesions in posterior part of the corpus callosum plus lesions of the left occipital
lobe can lead to

A

pure word blindness (alexia with no agraphia).

57
Q

Lesions of the posterior diencephalon and upper midbrain lead to

A

somnolence and hypersomnia.
Akinetic mutism may be seen where the patient is immobile and mute but has their eyes open.

58
Q

Obstructive lesions can lead to

A

intellectual decline secondary to raised intracranial pressure.

59
Q

Pseudobulbar palsy with extreme emotional lability may be seen

A

in bilateral lesions of the
corticobulbar tracts. The outward visible affect may be disconnected from the underlying emotion.

60
Q

Hypothalamic disturbances may cause

A

polydipsia, polyuria, hyperphagia, obesity and elevation of
temperature. There may be amenorrhoea or impotence in adults and delayed or precocious
puberty in children.

61
Q

If lesions involve the pituitary gland then

A

variety of endocrine changes- many of which have psychiatric sequalae

62
Q

Lesions of the thalamus are associated with

A

sensory disturbances such as those seen in parietal
lobe lesions. In addition there may be hyperalgesia or analgesia. Neuropathic pain has been treated
with deep brain stimulation of the ventral thalamic nuclei.

63
Q

Cognitive deficits (‘thalamic dementia’) may develop with

A

bilateral lesions of the thalamus.
Features include amnesia, confusion, affective flattening and apathy. Personality changes and hallucinations may also be seen

64
Q

What does the basal ganglia comprise?

A

caudate,
putamen, globus pallidus, substantia nigra,
ventral tegmental area, pedunculopontine
tegmental nucleus and subthalamic nucleus.

*striatum= caudate, putamen and nucleus accumbens

65
Q

What is the function of basal ganglia? and How?

A

Receive information from the cerebral cortex
and send back processed responses to this
information.

Basic process is through release of inhibition,
hence lesions result in release of behaviour
(e.g. uncontrolled movement of Parkinson’s
disease).

The ventral striatum contains the nucleus
accumbens, implicated in goal-directed
behaviour and the rewarding effects of
carbohydrates and drugs of abuse.

*function used to improve deep
brain stimulation (DBS) treatment of neurological andneuropsychiatric disorders.

66
Q

basal ganglia susceptible to damage in (what diseases)?

A

Huntington’s disease, Parkinson’s
disease, Wilson’s disease, heavy metal intoxication and
stroke.

*In Huntingdon’s disease, neurons are lost in the caudate,
putamen and ventral tegmental area. Depression commonly
antecedes other symptoms of Huntington’s disease.

67
Q

Basal ganglia lesions associated with variety of neuropsychiatric presentations, including

A

Tourette’s,
dementia, depression, obsessive-compulsive disorder
(OCD), apathy, aphasia, psychosis and mania.

68
Q

Lesions of the caudate nucleus produce

A

choreoathetosis on
the contralateral side, as well as abulia (apathy with loss of
spontaneous thought and emotion).

69
Q

What is the myoclonus dystonia syndrome?

A

where Obsessive-compulsive disorder linked to basal
ganglia pathology, as in the myoclonus dystonia
syndrome. Severe and disabling OCD, affecting their
functioning more than the movement disorder.

70
Q

What is Fahr’s syndrome?

A

calcification of the basal ganglia;
mood disorders, cognitive impairment, OCD and
psychosis.

71
Q

What is Wilson’s disease:

A

copper deposition in the liver, eyes and brain. Psychiatric symptoms; psychosis,
cognitive impairment and affective disorders.

72
Q

what is Pantothenate kinase-associated
neurodegeneration (PKAN)

A

(formerly called
Hallervorden-Spatz disease) is an autosomal
recessive disorder leading to parkinsonism,
dystonia, dementia, and ultimately death. “Eye of
the tiger” sign

73
Q

Basal ganglia have important functions in

A

regulation of attentional and cognitive functions,
and their pathology is linked neuropsychiatric
presentations.

74
Q

Role of cerebellum is

A

regulation of both
non-motor and motor function.

75
Q

Non-motor symptoms (cerebellar cognitive affective syndrome) results from + symptoms are

A

disrupted connections to the
cerebral cortex and limbic system

problems with
executive function, spatial
cognition, language and affect.
* Personality changes presenting
with blunting of affect or
disinhibition.

76
Q

Role of the brainstem is

A

Important roles in the regulation of
behaviour, cognition, and mood.

  • Forms the connection between the spinal
    cord, cerebellum and cerebrum
  • Many ascending and descending
    pathways, contains most cranial nerve
    nuclei and is important for many key
    integrative functions.
  • Source for monoamine neurotransmitter
    circuits projecting cortically.
77
Q

Major subdivisions of the brainstem (from
rostral to caudal) are

A

midbrain, pons,
and medulla.

78
Q

What is reticular formation?

A

contained in the
core of the brainstem. Phylogenetically
one of the oldest components of the brain
and is central to modulation of movement, pain, wakefulness, alertness
and arousal.

79
Q

What is the role of raphae nuclei?

A

The raphe nuclei positioned along the midline
of the medulla, pons and midbrain produce
serotonin; are implicated in control of sleep,
mood/affect, aggression and other

80
Q

where is pathological crying seen and how can it be treated?

A

Pathological crying is often seen after stroke,
and may be successfully treated with selective
serotonin reuptake inhibitor drugs, suggesting
that this results

81
Q

Ventral pons injuries can result in (what syndrome)?

A

characterized by paralysis of all four
limbs and paralytic mutism. Cognition may be
impaired: attention, memory difficulties as well
as deficits in mental calculation, problem
solving, auditory and visual recognition, and
receptive language.

82
Q

What are the lesions of deep midline structures

A

lesions of posterior diencephalon and upper midbrain, obstructive lesions, pseudobulbar palsy, hypothalamic disturbances, pituitary gland lesions, lesions of thalamus, cognitive deficits (thalamic dementia)

Mish- Scientific Foundations (6 decks)

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