Focal brain syndromes in neuropsychiatry

Question 1

What does the frontal lobe consist of?

Answer 1

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

Question 2

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

Answer 2

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

Question 3

What neuropsychiatric tests are done for dorsolateral prefrontal cortex lesions?

Answer 3

Similarities/differences test

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

Question 4

What are the causes of dorsolateral prefrontal cortex lesions?

Answer 4

Tumours, cerebrovascular accidents and frontal neurodegeneration

Question 5

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

Answer 5

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

Question 6

What are the physical symptoms of orbital prefrontal cortex lesions?

Answer 6

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

Question 7

What are the causes of orbital prefrontal cortex lesions?

Answer 7

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

Question 8

What are the psychiatric symptoms associated with medial prefrontal cortex?

Answer 8

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

Question 9

Bilateral lesions lead to

Answer 9

akinetic mutism

Question 10

What are the causes of medial prefrontal cortex lesions?

Answer 10

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

Question 11

What clinical tests are used for frontal lobe function determination?

Answer 11

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

Question 12

What are the roles of the parietal lobe?

Answer 12

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

Question 13

parietal lobe anatomically underlies

Answer 13

the parietal bone of the skull

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

Question 14

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

Answer 14

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

Question 15

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

Answer 15

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

Question 16

Distinguish between where primary motor and sensory dysphasias occur?

Answer 16

primary motor dysphasia= anterior lesion

primary sensory dysphasia = posterior lesions

Question 17

which lesion causes visual agnosia

Answer 17

posterior lesions (parieto-occipital)

Question 18

what are the neurological features of parietal lobe lesions?

Answer 18

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

Question 19

What clinical tests are used for parietal lobe function?

Answer 19

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

Question 20

Temporal lobe divided into

Answer 20

lateral and ventromedial

Question 21

lateral region is

Answer 21

neocortex and has multiple cognitive functions.

Question 22

ventromedial region contains

Answer 22

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

Question 23

function of temporal lobe is

Answer 23

• (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?)

Question 24

What are the psychiatric symptoms of dominant temporal lobe lesions?

Answer 24

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.

Question 25

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

Answer 25

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).

Question 26

What emotions are seen during temporal lobe seizure?

Answer 26

- fear, - anxiety, - pleasure, - depersonalisation, - depression, - déjà vu (familiarity) and jamais vu (unfamiliarity).

Question 27

Where is olfactory cortex located?

Answer 27

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.

Question 28

Symptoms of epileptic seizures and where it affects?

Answer 28

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

Question 29

Features of mesial temporal seizures include

Answer 29

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

Question 30

Seizures affecting the middle and inferior temporal gyri cause

Answer 30

complex hallucinations or aberrant salience attribution to neutral perceptions (delusion attributed to perception)

Question 31

Other temporal lobe syndromes include

Answer 31

Bilateral hippocampal lesions and Kluver-Bucy syndrome

Question 32

What are the symptoms of Bilateral hippocampal lesions?

Answer 32

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.

Question 33

Symptoms of Kluver-Bucy syndrome are

Answer 33

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.

Question 34

Kluver-Bucy syndrome caused by what lesion?

Answer 34

bilateral medial temporal lobe lesions.

Question 35

What are the causes of temporal lobe syndromes?

Answer 35

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

Question 36

How does loss of fear occur (anatomically)?

Answer 36

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

Question 37

Deeper lesions within the temporal lobe (anatomically) cause

Answer 37

contralateral homonymous upper quadrant field defects, due to damage to the visual radiation. * May also be mild contralateral hemiparesis due to corona radiata damage.

Question 38

What are the clinical tests for temporal lobe function?

Answer 38

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

Question 39

What (anatomically) distinguishes the occipital lobe from parietal?

Answer 39

on the medial surface by the parieto-occipital sulcus.

Question 40

What is the function of the occipital lobe?

Answer 40

Primarily concerned with higher order visual processing. * Process complex information about the form, motion, colour and depth of perceived objects.

Question 41

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

Answer 41

Relatively common lesions- (posterior cortical artery strokes 5%) primary visual cortex lesions= visual blind spots (scotomas) & partial blind spots (amblyopias)

Question 42

Bilateral lesions of occipital cortex lead to

Answer 42

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

Question 43

What is seen with extensive bilateral occipital cortex lesions?

Answer 43

* 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).

Question 44

Lesions of the dominant occipital lobe lead to

Answer 44

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

Question 45

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

Answer 45

BA19

Question 46

Bilateral occipitoparietal lesions may cause

Answer 46

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

Question 47

What is posterior cortical atrophy?

Answer 47

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

Question 48

What is posterior cortical atrophy caused by?

Answer 48

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

Question 49

What other disorders affect the occipital lobe?

Answer 49

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.

Question 50

Irritation or damage to visual association cortex causes

Answer 50

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

Question 51

What is polyopsia and palinopsia?

Answer 51

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.

Question 52

What are occipital lobe function tests?

Answer 52

* 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

Question 53

What can complete callosal damage lead to?

Answer 53

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.

Question 54

after callosectomy there is often

Answer 54

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

Question 55

lesions of anterior corpus callosum lead to (symptom)

Answer 55

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

Question 56

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

Answer 56

pure word blindness (alexia with no agraphia).

Question 57

Lesions of the posterior diencephalon and upper midbrain lead to

Answer 57

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

Question 58

Obstructive lesions can lead to

Answer 58

intellectual decline secondary to raised intracranial pressure.

Question 59

Pseudobulbar palsy with extreme emotional lability may be seen

Answer 59

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

Question 60

Hypothalamic disturbances may cause

Answer 60

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

Question 61

If lesions involve the pituitary gland then

Answer 61

variety of endocrine changes- many of which have psychiatric sequalae

Question 62

Lesions of the thalamus are associated with

Answer 62

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.

Question 63

Cognitive deficits ('thalamic dementia') may develop with

Answer 63

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

Question 64

What does the basal ganglia comprise?

Answer 64

caudate, putamen, globus pallidus, substantia nigra, ventral tegmental area, pedunculopontine tegmental nucleus and subthalamic nucleus. *striatum= caudate, putamen and nucleus accumbens

Question 65

What is the function of basal ganglia? and How?

Answer 65

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.

Question 66

basal ganglia susceptible to damage in (what diseases)?

Answer 66

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.

Question 67

Basal ganglia lesions associated with variety of neuropsychiatric presentations, including

Answer 67

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

Question 68

Lesions of the caudate nucleus produce

Answer 68

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

Question 69

What is the myoclonus dystonia syndrome?

Answer 69

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.

Question 70

What is Fahr's syndrome?

Answer 70

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

Question 71

What is Wilson's disease:

Answer 71

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

Question 72

what is Pantothenate kinase-associated neurodegeneration (PKAN)

Answer 72

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

Question 73

Basal ganglia have important functions in

Answer 73

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

Question 74

Role of cerebellum is

Answer 74

regulation of both non-motor and motor function.

Question 75

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

Answer 75

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.

Question 76

Role of the brainstem is

Answer 76

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.

Question 77

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

Answer 77

midbrain, pons, and medulla.

Question 78

What is reticular formation?

Answer 78

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.

Question 79

What is the role of raphae nuclei?

Answer 79

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

Question 80

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

Answer 80

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

Question 81

Ventral pons injuries can result in (what syndrome)?

Answer 81

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.

Question 82

What are the lesions of deep midline structures

Answer 82

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