Neurology- Movement Disorders/Brain Lesions/Strokes/etc. Flashcards

1
Q

What is athetosis and what commonly causes it?

A

slow, writhing, snake-like movements, especially in the fingers due to lesions of basal ganglia (e.g. Huntington)

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2
Q

What is chorea and what commonly causes it?

A

sudden, jerky, purposeless movements due to lesion of basal ganglia (e.g. Huntington)

chorea= dancing

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3
Q

What is an dystonia and what commonly causes it?

A

sustained, involuntary muscle contractions (exs: Writer’s cramp; blepharospasm (sustained eyelid twitch)

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4
Q

What is an essential tremor and what commonly causes it?

A

a high-frequency tremor with sustained posture (e.g. outstretched arms), worsened with movement or anxiety

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5
Q

How can essential tremor be tx?

A

EtOH (probably not healthy)

BBs and primidone

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6
Q

What is hemiballimus and what commonly causes it?

A

sudden, wild flailing of 1 arm +/- ipsilateral leg caused by a contralateral subthalamic nucleic lesion (e.g. lacunar stroke)

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7
Q

What is an intention tremor and what commonly causes it?

A

a slow, zigzag motion when pointing/extending toward a target caused by cerebellar dysfunction

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8
Q

What is myoclonus and what commonly causes it?

A

sudden, brief, uncontrolled muscle contraction common in metabolic abnormlaities such as renal or liver failure

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9
Q

What is a resting tremor and what commonly causes it?

A

uncontrolled movement of distal appendages that is alleviated by intentional movement

Commonly seen in Parkinson disease

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10
Q

What are the symptoms of Parkinson disease?

A

TRAPS

Tremor (pill-rolling tremor at rest)

Rigidity

Akinesia

Postural instability

Shuffling gait

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11
Q

Parkinson is a degenerative disorder of the CNS associated with what histologic findings?

A

Lewy bodies, composed of a-synuclein (intracellular eosinophilic inclusions) (below)

and loss dopaminergic neurons (ie. depigmentation) of substantia migra pars compacts

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12
Q

What causes Huntington disease?

A

AD trinucleotide repeat disorder on chromosome 4 leads to neuronal death via NMDA-R binding and glutamate toxicity

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13
Q

When does Huntington typically present first?

A

20-50 yo

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14
Q

How does Huntington present initially?

A

choreiform movements, depression, aggression, and/or dementia

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15
Q

What lab values are indicative of Huntington disease?

A

elevated dopamine

decreased GABA and Ach

in brain

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16
Q

What is aphasia?

A

the inability to speak or understand language caused by brain damage

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17
Q

What is dysarthria?

A

Dysarthria is a motor speech disorder resulting from neurological injury of the motor component of the motor-speech system and is characterized by poor articulation of phonemes.

In other words, it is a condition in which problems effectively occur with the muscles that help produce speech, often making it very difficult to pronounce words. It is unrelated to any problem with understanding cognitive language. Any of the speech subsystems (respiration, phonation, resonance, prosody, and articulation) can be affected, leading to impairments in intelligibility, audibility, naturalness, and efficiency of vocal communication.

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18
Q

Dysarthria that has progressed to a total loss of speech is referred to as ______

A

anarthria.

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19
Q

What are some major types of aphasia?

A
  • Broca
  • Wernicke
  • Conduction
  • Global
  • Transcortical motor
  • Transcortical sensory
  • Mixed transcortical

need to do all of pg 460

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20
Q

What would a bilateral lesion to the amygdala cause?

A

Kluver-Bucy syndrome-disinhibited behavior (e.g. hyperphagia, hypersexualityi, hyperorality)

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21
Q

Bilateral lesion to the amygdala is associated with what?

A

HSV-1

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22
Q

Lesion to the frontal lobe causes what?

A

Disinhibition and deficits in concentration, orientation, and judgement; pts may have reemergence of primitive reflexes

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23
Q

Lesions of the nondominant parietal-temporal cortex cause what?

A

hemispatial neglect syndrome (agnosai of the contralateral side of the world)

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24
Q

Lesions of the dominant parietal-temporal cortex cause what?

A

Gerstmann syndrome:

agraphia (An acquired neurological disorder causing a loss in the ability to communicate through writing, either due to some form of motor dysfunction or an inability to spell)

acalculia (loss of the ability to perform simple arithmetic calculations)

finger agnosia

left-right disorientation

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25
Q

What is finger agnosia?

A

the loss in the ability “to distinguish, name, or recognize the fingers”, not only with the patient’s own fingers, but also the fingers of others, and drawing and other representations of fingers

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26
Q

Lesion of the reticular activating system (midbrain) leads to what?

A

reduced levels of arousal and wakefullness (e.g. coma)

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27
Q

Lesion of the mammillary bodies (bilateral) leads to what?

A

Wernicke-Korsakoff syndrome, marked by confusion, ophthalmoplegia, ataxia, memory loss, confabulation, and personality changes

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28
Q

What is confabulation?

A

a disturbance of memory, defined as the production of fabricated, distorted or misinterpreted memories about oneself or the world, without the conscious intention to deceive.

Individuals who confabulate present incorrect memories ranging from “subtle alterations to bizarre fabrications”, and are generally very confident about their recollections, despite contradictory evidence

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29
Q

What is ophthalmoplegia?

A

paralysis of the muscles within or surrounding the eye.

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30
Q

Wernicke-Korsakoff syndrome is associated with what?

A

thaimine (B1) deficiency and excessive EtOH use

can be precipitated by giving gluocse without B1 to a B1-deficiency pt.

Wernicke problems come in a CAN of beer: Confusion, Ataxia, and Nystagmus

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31
Q

Lesion of the basal ganglia can lead to what?

A

tremor at rest, chorea, or athetosis (e.g. Parkinson or Huntington)

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32
Q

Lesion to a cerebellar hemisphere can lead to what?

A

intention tremor, limb ataxia, loss of balance

typically damage to the cerebellum leads to ipsilateral deficits and falls TOWARD the side of the lesion

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33
Q

Lesion to the cerebellar vermus can lead to what?

A

truncal ataxia, dysathria (slurred or slow speech that can be difficult to understand)

the Vermis centrally located and affects the central body

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34
Q

Lesion of the subthamaic nucleus can lead to what?

A

contralateral hemiballismus

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35
Q

Bilateral lesion of the hippocampus can lead to what?

A

anterograde amensia- inability to make NEW memories

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36
Q

Lesion of the paramedian pontine retuclar formation can lead to what?

A

the eyes look away from the side of the lesion

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37
Q

Lesion of the frontal eye fields can lead to what?

A

the eyes look TOWARD the lesion side

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38
Q

Study the distribution of the cerebral arteries on pg 462

A
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39
Q

What are the watershed zones of the cerebral aa.?

A

between the anterior and middle cerebral, and posterior and middle cerebral aa.

Damage in severe hypotension can lead to upper leg and upper arm weakness, and defects in higher-order visual processing

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40
Q

The anterior and middle cerebral aa. branch from what artery?

A

ICA

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41
Q

What connects the two anterior cerebral aa. in front of the optic chiasm?

A

the anterior communicating a.

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42
Q

What connects the middle cerebral aa. with the posterior cerebral aa. on each side?

A

the posterior communicating aa. (1 on each side)

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43
Q

What gives rise to the posterior cerebral aa.?

A

two vertebral aa. combine to form a basilar a. which then branches many times, the last of each are the two posterior cerebral aa.

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44
Q

Brain perfusion relies on tight autoregulation. What drives cerebral perfusion?

A

PCo2 (and some PO2 in severe hypoxia)

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45
Q

Hypoexmia inreases cerebral perfusion pressure only when PO2 drops to what?

A

below 50 mmHg

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46
Q

So, increasing PCo2 increases cerebral perfusion linearly until greater than 90mmHg

A
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47
Q

NOTE: Therapeutic hyperventilation (decreases PCO2) helps decrease intracranial pressure (ICP) in cases of acute cerebral edema (Stroke, trauma) via vasocontriction.

A

Fainting in panic attacks is caused by decreased perfusion

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48
Q

What else does cerebral perfusion rely on?

A

a pressure gradient between MAP and ICP.

CPP= MAP- ICP. Decreased MAP or increased ICP decreases cerebral perfusion pressure (CPP)

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49
Q

What happens if CPP=0?

A

brain death

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50
Q
A
51
Q

The three major sources of stroke claudication in the anterior brain circulation are:

A
  • MCA
  • ACA
  • Lenticulostriate artery
52
Q

How would stroke to the motor cortex caused by MCA claudication present?

A

contralateral paralysis- upper limb and face

53
Q

How would stroke to the sensory cortex caused by MCA claudication present?

A

contralateral loss of sensation to the upper limb and face

54
Q

How would stroke to the temporal lobe (Wernicke area)/ frontal lobe (Broca) caused by MCA claudication present?

A

aphasia if in the dominant (usually left) hemisphere. Hemineglect if lesion affect the nondominant side

55
Q

How would stroke to the motor cortex caused by ACA claudication present?

A

contralalteral paralysis of the lower limb

56
Q

How would stroke to the sensory cortex caused by ACA claudication present?

A

contralateral loss of sensation in the lower limb

57
Q

How would stroke to the striatum/internal capsule caused by lenticulostriate a. claudication present?

A

contralateral hemiparesis/hemiplegia (paralysis of one side of the body.)

Hemiparesis is unilateral paresis, that is, weakness of the entire left or right side of the body (hemi- means “half”). Hemiplegia is, in its most severe form, complete paralysis of half of the body

58
Q

The lenticulostriate a is a common location of _______ infarcts

A

lacunar; secondary to unmanaged HTN

59
Q

The three major sources of stroke claudication in the posterior brain circulation are:

A
  • ASA
  • PICA
  • AICA
  • PCA
  • Basilary a.
60
Q

How would stroke to the lateral corticospinal tract caused by ASA claudication present?

A

contralateral hemiparesis-upper and lower limbs

61
Q

How would stroke to the medial lemniscus caused by ASA claudication present?

A

decreased contralateral proprioception

62
Q

How would stroke to the caudal medulla (hypoglossal nerve) caused by ASA claudication present?

A

ipsilateral hypoglossal dysfunction (tongue deviates to the side of the lesion)

63
Q

T or F. Stroke caused by ASA claudication is usually bilateral

A

T.

64
Q

What is Medial medullary syndrome?

A

caused by infarct of paramedian branches of the ASA and vertebral aa.

65
Q

How would stroke to the lateral medulla (vestibular nuclei, lateral sponthalamic tract, spinal trigemeninal nucleus, nucleus ambiguus, sympathetic fibers, and inferior cerebellar peduncle) caused by PICA claudication present?

A

as Lateral medullary (Wallenberg) syndrome

vomiting, vertigo, nystagmus

decreased pain and temp sensation from the ipsilateral face and contralateral body

dysphagia

hoarseness

decreased gag reflex

ipsilateral Horner syndrome

ataxis and dysmetria

66
Q

What is dysmetria?

A

refers to a lack of coordination of movement typified by the undershoot or overshoot of intended position with the hand, arm, leg, or eye. It is a type of ataxia. It is sometimes described as an inability to judge distance or scale.

67
Q

______ effects ae specific to PICA lesions

A

Nucleus ambiguus

68
Q

How would stroke to the lateral pons (cranial nerve nuclei, vestibular nuclei, facial nucleus, spinal trigeminal nucleus, cochlear nuclei, and sympathetic fibers) caused by AICA claudication present?

A

Lateral pontine syndrome

vomiting, vertigo, nystagmus

paralysis of the face

decreased lacrimation and salivation

decreased taste from the anterior 2/3 of tongue

decreased ipsilateral pain and temp sensation on the face and decreased contralateral pain and temp sensation on the body

69
Q

How would stroke to the middle and inferior cerebellar peduncles caused by AICA claudication present?

A

ataxia and dysmetria

70
Q

How would stroke to the occipital cortex and visual cortex caused by PICA claudication present?

A

contralateral hemianopia with macular sparing

71
Q

How would stroke to the pons, medulla, lower midbrain, corticospinal and corticobulbar tracts, ocular CN nuclei, and paramedian pontine reticular formation caused by Basilar a. claudication present?

A

“Locked-In syndrome”

preserved consciousness and blinking,

quadriplegia

loss of voluntary facial, mouth, and tongue movements

72
Q

The two major sources of stroke claudication in the communicating brain circulation are:

A

ACom and PCom

73
Q

What is the most common lesion of the ACom?

A

aneurysm (can lead to stroke)

NOTE: Saccular (berry) aneurysm can impinge cranial nerves

74
Q

How would lesion to the ACom present?

A

visual field defects (note that most lesions are aneuryms, not strokes)

75
Q

_____ is a common site for saccular aneurysms

A

PCom

76
Q

How would a PCom lesion (again, mostly aneurysms) present?

A

CN III palsy- eye is ‘down and out” with ptosis and mydriasis

77
Q

Where do Saccular (berry) aneurysms occur?

A

At birfurcations in the circle of Willis, most commonly at the junction of the ACom and anterior cerebral artery

78
Q

Rupture, the most common complication of a berry aneurysm, can cause what?

A

subarachnoid hemorrhage (aka “worst HA of my life”) or hemorrhagic stroke

can also cause bitemporal hemianopia via compression of the optic chiasm

79
Q

berry aneurysms are associated with what?

A

ADPKD, Ehlers-Danlos syndrome

advanced age, HTN, smoking, AA race

80
Q

What is a Charcot-Bouchard microaneurysm?

A

aneurysm of small vessels (e.g. in basal ganglia, thalamus); associated with chronic HTN

81
Q

What is Central post-stroke pain syndrome?

A

neuropathic pain due to thalamic lesions. Initial paresthesias followed in weeks-months by allodynia (oridinarily painless stimuli cause pain) and dysethesia (defined as an unpleasant, abnormal sense of touch. It often presents as pain, but may also present as an inappropriate, but not discomforting, sensation.)

Occurs in 10% of stroke pts

82
Q

What is this?

A

an epidural hematoma, caused by rupture of middile meningeal artery (branch of the maxillary a.), often secondary to fracture of the temporal bone

83
Q

How might an epidural hematoma present?

A

lucid intervals

rapid expansion under pressure can lead to transtentorial herniation

CN III palsy

84
Q

Describe the CT of an epidural hematoma

A

CT shows biconvex (lentiform), hyperdense blood collection, not crossing suture lines.

Can cross falx, tenorium

85
Q

What is this?

A

A subdural hematome, caused by rupture of bridging veins resulting in slow venous bleeding (less pressure=slowly developing)

86
Q

A subdural hematoma is commonly seen in who?

A

elderly, alcoholics, blunt trauma, shaken baby

87
Q

Describe the CT of a subdural hematoma

A

crescent shaped that does cross suture lines and causes a midline shift

Cannot cross the falx or tentorium

88
Q

What is this?

A

A subarachnoid hemorrhage, caused by rupture of an aneurysm as seen commonly in Ehlers-Danlos or arteriovenous malformation and progressing rapidly to present with the ‘worst HA of my life”

89
Q

Intraparenchymal (HTN) hemorrhage is most commonly caused by systemic HTN, but is also seen in what?

A

angiopathy (recurrent lobar hemorrhagic stroke in elderly), vasculitis, or neoplasm

90
Q

Where does Intraparenchymal (HTN) hemorrhage typically occur?

A

basal ganglia and internal capsule (in the case of charcot-Bouchard aneurysm), but can be lobar

91
Q

Irreversible damage from ischemic brain disease/stroke occurs when?

A

after 5 minutes of hypoxia

92
Q

What are the most vulnerable parts of the brain to stroke?

A

hippocampus, neocortex, cerebellum, and watershed areas

93
Q

What imaging should be used for a stroke?

A

noncontrast CT to exclude hemorrhage (before tPA can be given)

CT detects ischemic changes in 6-24 hrs

Diffusion weighted MI can detect ischemia within 3-30 min

94
Q

What is the main histo feature 12-48 hrs after stroke?

A

red neurons

95
Q

What is the main histo feature 24-72 hrs after stroke?

A

necrosis and neutrophils

96
Q

What is the main histo feature 3-5 days after stroke?

A

macrophages (microglia)

97
Q

What is the main histo feature 1-2 weeks after stroke?

A

reactive gliosis and vascular proliferation

98
Q

What is the main histo feature 2+ weeks after stroke?

A

a glial scar

99
Q

What is hemorrhagic stroke?

A

intracerebral bleeding, often due to HTN, anticoagulation, cancer (abnormal vessels can bleed). May also be secondary to ischemic stroke followed by reperfusion (which increases vessel fragility)

100
Q

What is the most common site of intracerebral hemorrhage?

A

basal ganglia

101
Q

Ischemic stroke is caused by the acute blockage of vessels causing disruption of blood flow and subsequent ischemia leading to liquefactive necrosis

A
102
Q

What are the three types of ischemic stroke?

A
  • Thrombotic
  • Embolic
  • Hypoxic
103
Q

Describe thrombotic ischemic stroke

A

due to a clot forming directly at the site of infarction (commonly the MCA) usually over an atherosclerotic plaque

104
Q

What are common causes of embolic ischemic stroke?

A

a. fib, DVT with a patent foramen ovale

105
Q

What is the tx for ischemic stroke?

A

tPA (if within 3-4.5 hr of onset and no hemorrhage/risk of hemorrhage)

Reduce further risk with medical therapy (e.g. aspirin, clopidogrel)

optimum control of BP, blood sugar, and lipids

106
Q

What is a transient ischemic attack?

A

brief, reversible episode of focal neurologic dysfunction without acute infarct (negative MRI) with the majority resolving in less than 15 minutes

deficits due to focal ischemia

107
Q

Dural venous sinuses drain blood from cerebral veins and receive CSF from arachnoid granulations. What do they drain into?

A

internal jugular veins

pg 467

108
Q

Where is CSF made?

A

by ependymal cells in the choroid plexus

109
Q

Describe the path of CSF

A

made in the lateral ventricles, and drain to the 3rd ventricle via the Foramen of Monro, then to the 4th ventricle via the cerebral aqueduct of Sulvius

110
Q

Where does 4th ventricle CSF flow?

A

to the subarachnoid space via the:

foramine of Luschka (lateral)

foramen of Magendie (medial)

111
Q

What is idiopathic intracranial HTN (pseudotumor cerebri)?

A

increased ICP with no apparnt cause on imaging (ie.. hydrocephalus, obstruction of CSF outflow)

112
Q

How does a idiopathic intracranial HTN (pseudotumor cerebri) present?

A

with HA, diplopia (usually from CN VI palsy)

no mental status alcerations

papilledema seen on exam

113
Q

What are the risk factors of idiopathic intracranial HTN (pseudotumor cerebri)?

A

woman of childbearing age

vitamin A excess

danazol

114
Q

How is idiopathic intracranial HTN (pseudotumor cerebri) tx?

A

lumbar puncture can relieve pressure

weight loss

acetazolamide

topiramate

invasive procedures for refractory cases (e.g. repeat lumbar puncture, CSF shunt placement, optic nerve fenestration surgery)

115
Q

What is hydrocephalus?

A

Hydrocephalus is a condition in which there is an abnormal accumulation of cerebrospinal fluid (CSF) within the brain. This typically causes increased pressure inside the skull. Older people may have headaches, double vision, poor balance, urinary incontinence, personality changes, or mental impairment. In babies there may be a rapid increase in head size. Other symptoms may include vomiting, sleepiness, seizures, and downward pointing of the eyes

116
Q

What are the types of hydrocephalus?

A
  • communicating (nonobstructive): communicating and normal pressure
  • noncommunicating (obstructive)
117
Q

What causes communicating hydrocephalus?

A

decreased CSF absorption by arachnoid granulation leading to increased ICP, papilledema, and herniation

118
Q

What causes normal pressure hydrocephalus?

A

In the elderly, idiopathic in nature; CSF pressure elevated only episodically

does not result in increased subarachnoid space volume

119
Q

How does normal pressure hydrocephalus present?

A

expanson of ventricles distorts the fibers of the corona radiata leading to the classic triad of: urinary incontinence, ataxia, and cognitive dysfunction

“Wet, wobbly, and wacky”

120
Q

What causes a noncommunicating hydrocephalus?

A

caused by structural blockage of CSF circulation within the ventricular system (e.g. stenosis of the aqueduct of Sylvius; colloied cyst blocking the foramen of Monro)

121
Q

What is ex vacuo ventriculomegaly?

A

the appearance of increased CSF on imaging, actually due to decreased brain tissue (neuronal atrophy) (in cases of Alzheimer disease, advanced HIV, Pick disease)

triad not seen

122
Q

What is Pick disease?

A

Pick’s disease, a type of frontotemporal dementia, is a rare neurodegenerative disease that causes progressive destruction of nerve cells in the brain.

Common symptoms that are noticed early on in the diagnosis are personality and emotional changes, as well as, deterioration of language. Many who are diagnosed with Pick’s disease can be impulsive, apathetic, and euphoric. While some of the symptoms can initially be alleviated, the disease progresses and patients often die within two to ten years.

123
Q

What is a classic finding of Pick disease?

A

A defining characteristic of the disease is build-up of tau proteins in neurons, accumulating into silver-staining, spherical aggregations known as “Pick bodies”