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)
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
3
Q
What is an dystonia and what commonly causes it?
A
sustained, involuntary muscle contractions (exs: Writer’s cramp; blepharospasm (sustained eyelid twitch)
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
5
Q
How can essential tremor be tx?
A
EtOH (probably not healthy)
BBs and primidone
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)
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
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
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
10
Q
What are the symptoms of Parkinson disease?
A
TRAPS
Tremor (pill-rolling tremor at rest)
Rigidity
Akinesia
Postural instability
Shuffling gait
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
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
13
Q
When does Huntington typically present first?
A
20-50 yo
14
Q
How does Huntington present initially?
A
choreiform movements, depression, aggression, and/or dementia
15
Q
What lab values are indicative of Huntington disease?
A
elevated dopamine
decreased GABA and Ach
in brain
16
Q
What is aphasia?
A
the inability to speak or understand language caused by brain damage
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.
18
Q
Dysarthria that has progressed to a total loss of speech is referred to as ______
A
anarthria.
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
20
Q
What would a bilateral lesion to the amygdala cause?
A
Kluver-Bucy syndrome-disinhibited behavior (e.g. hyperphagia, hypersexualityi, hyperorality)
21
Q
Bilateral lesion to the amygdala is associated with what?
A
HSV-1
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
23
Q
Lesions of the nondominant parietal-temporal cortex cause what?
A
hemispatial neglect syndrome (agnosai of the contralateral side of the world)
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
25
What is finger agnosia?
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
26
Lesion of the reticular activating system (midbrain) leads to what?
reduced levels of arousal and wakefullness (e.g. coma)
27
Lesion of the mammillary bodies (bilateral) leads to what?
**Wernicke-Korsakoff syndrome**, marked by confusion, ophthalmoplegia, ataxia, memory loss, confabulation, and personality changes
28
What is confabulation?
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
29
What is ophthalmoplegia?
paralysis of the muscles within or surrounding the eye.
30
Wernicke-Korsakoff syndrome is associated with what?
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**
31
Lesion of the basal ganglia can lead to what?
tremor at rest, chorea, or athetosis (e.g. Parkinson or Huntington)
32
Lesion to a cerebellar hemisphere can lead to what?
intention tremor, limb ataxia, loss of balance
typically damage to the cerebellum leads to ipsilateral deficits and falls TOWARD the side of the lesion
33
Lesion to the cerebellar vermus can lead to what?
truncal ataxia, dysathria (slurred or slow speech that can be difficult to understand)
the Vermis centrally located and affects the central body
34
Lesion of the subthamaic nucleus can lead to what?
contralateral hemiballismus
35
Bilateral lesion of the hippocampus can lead to what?
**anterograde amensia**- inability to make NEW memories
36
Lesion of the paramedian pontine retuclar formation can lead to what?
the eyes look away from the side of the lesion
37
Lesion of the frontal eye fields can lead to what?
the eyes look TOWARD the lesion side
38
Study the distribution of the cerebral arteries on pg 462
39
What are the watershed zones of the cerebral aa.?
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
40
The anterior and middle cerebral aa. branch from what artery?
ICA
41
What connects the two anterior cerebral aa. in front of the optic chiasm?
the anterior communicating a.
42
What connects the middle cerebral aa. with the posterior cerebral aa. on each side?
the posterior communicating aa. (1 on each side)
43
What gives rise to the posterior cerebral aa.?
two vertebral aa. combine to form a basilar a. which then branches many times, the last of each are the two posterior cerebral aa.
44
Brain perfusion relies on tight autoregulation. What drives cerebral perfusion?
PCo2 (and some PO2 in severe hypoxia)
45
Hypoexmia inreases cerebral perfusion pressure only when PO2 drops to what?
below 50 mmHg
46
So, increasing PCo2 increases cerebral perfusion linearly until greater than 90mmHg
47
NOTE: Therapeutic hyperventilation (decreases PCO2) helps decrease intracranial pressure (ICP) in cases of acute cerebral edema (Stroke, trauma) via vasocontriction.
Fainting in panic attacks is caused by decreased perfusion
48
What else does cerebral perfusion rely on?
a pressure gradient between MAP and ICP.
CPP= MAP- ICP. Decreased MAP or increased ICP decreases cerebral perfusion pressure (CPP)
49
What happens if CPP=0?
brain death
50
51
The three major sources of stroke claudication in the anterior brain circulation are:
- MCA
- ACA
- Lenticulostriate artery
52
How would stroke to the motor cortex caused by MCA claudication present?
contralateral paralysis- upper limb and face
53
How would stroke to the sensory cortex caused by MCA claudication present?
contralateral loss of sensation to the upper limb and face
54
How would stroke to the temporal lobe (Wernicke area)/ frontal lobe (Broca) caused by MCA claudication present?
aphasia if in the dominant (usually left) hemisphere. Hemineglect if lesion affect the nondominant side
55
How would stroke to the motor cortex caused by ACA claudication present?
contralalteral paralysis of the lower limb
56
How would stroke to the sensory cortex caused by ACA claudication present?
contralateral loss of sensation in the lower limb
57
How would stroke to the striatum/internal capsule caused by lenticulostriate a. claudication present?
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
The lenticulostriate a is a common location of _______ infarcts
lacunar; secondary to unmanaged HTN
59
The three major sources of stroke claudication in the posterior brain circulation are:
- ASA
- PICA
- AICA
- PCA
- Basilary a.
60
How would stroke to the lateral corticospinal tract caused by ASA claudication present?
contralateral hemiparesis-upper and lower limbs
61
How would stroke to the medial lemniscus caused by ASA claudication present?
decreased contralateral proprioception
62
How would stroke to the caudal medulla (hypoglossal nerve) caused by ASA claudication present?
ipsilateral hypoglossal dysfunction (tongue deviates to the side of the lesion)
63
T or F. Stroke caused by ASA claudication is usually bilateral
T.
64
What is Medial medullary syndrome?
caused by infarct of paramedian branches of the ASA and vertebral aa.
65
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?
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
What is dysmetria?
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
\_\_\_\_\_\_ effects ae specific to PICA lesions
Nucleus ambiguus
68
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?
**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
How would stroke to the middle and inferior cerebellar peduncles caused by AICA claudication present?
ataxia and dysmetria
70
How would stroke to the occipital cortex and visual cortex caused by PICA claudication present?
contralateral hemianopia with macular sparing
71
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?
**"Locked-In syndrome"**
preserved consciousness and blinking,
quadriplegia
loss of voluntary facial, mouth, and tongue movements
72
The two major sources of stroke claudication in the communicating brain circulation are:
ACom and PCom
73
What is the most common lesion of the ACom?
aneurysm (can lead to stroke)
NOTE: Saccular (berry) aneurysm can impinge cranial nerves
74
How would lesion to the ACom present?
visual field defects (note that most lesions are aneuryms, not strokes)
75
\_\_\_\_\_ is a common site for saccular aneurysms
PCom
76
How would a PCom lesion (again, mostly aneurysms) present?
CN III palsy- eye is 'down and out" with ptosis and mydriasis
77
Where do Saccular (berry) aneurysms occur?
At birfurcations in the circle of Willis, most commonly at the **junction of the ACom and anterior cerebral artery**
78
Rupture, the most common complication of a berry aneurysm, can cause what?
subarachnoid hemorrhage (aka "worst HA of my life") or hemorrhagic stroke
can also cause bitemporal hemianopia via compression of the optic chiasm
79
berry aneurysms are associated with what?
ADPKD, Ehlers-Danlos syndrome
advanced age, HTN, smoking, AA race
80
What is a Charcot-Bouchard microaneurysm?
aneurysm of **small vessels** (e.g. in basal ganglia, thalamus); _associated with chronic HTN_
81
What is Central post-stroke pain syndrome?
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
What is this?
an epidural hematoma, caused by rupture of middile meningeal artery (branch of the maxillary a.), often secondary to fracture of the temporal bone
83
How might an epidural hematoma present?
lucid intervals
rapid expansion under pressure can lead to transtentorial herniation
CN III palsy
84
Describe the CT of an epidural hematoma
CT shows biconvex (lentiform), hyperdense blood collection, not crossing suture lines.
**Can** cross falx, tenorium
85
What is this?
A subdural hematome, caused by rupture of bridging veins resulting in slow venous bleeding (less pressure=slowly developing)
86
A subdural hematoma is commonly seen in who?
elderly, alcoholics, blunt trauma, shaken baby
87
Describe the CT of a subdural hematoma
crescent shaped that does cross suture lines and causes a midline shift
Cannot cross the falx or tentorium
88
What is this?
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
Intraparenchymal (HTN) hemorrhage is most commonly caused by systemic HTN, but is also seen in what?
angiopathy (recurrent lobar hemorrhagic stroke in elderly), vasculitis, or neoplasm
90
Where does Intraparenchymal (HTN) hemorrhage typically occur?
basal ganglia and internal capsule (in the case of charcot-Bouchard aneurysm), but can be lobar
91
Irreversible damage from ischemic brain disease/stroke occurs when?
after 5 minutes of hypoxia
92
What are the most vulnerable parts of the brain to stroke?
hippocampus, neocortex, cerebellum, and watershed areas
93
What imaging should be used for a stroke?
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
What is the main histo feature 12-48 hrs after stroke?
red neurons
95
What is the main histo feature 24-72 hrs after stroke?
necrosis and neutrophils
96
What is the main histo feature 3-5 days after stroke?
macrophages (microglia)
97
What is the main histo feature 1-2 weeks after stroke?
reactive gliosis and vascular proliferation
98
What is the main histo feature 2+ weeks after stroke?
a glial scar
99
What is hemorrhagic stroke?
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
What is the most common site of intracerebral hemorrhage?
basal ganglia
101
Ischemic stroke is caused by the acute blockage of vessels causing disruption of blood flow and subsequent ischemia leading to **liquefactive necrosis**
102
What are the three types of ischemic stroke?
- Thrombotic
- Embolic
- Hypoxic
103
Describe thrombotic ischemic stroke
due to a clot forming directly at the site of infarction (commonly the MCA) usually over an atherosclerotic plaque
104
What are common causes of embolic ischemic stroke?
a. fib, DVT with a patent foramen ovale
105
What is the tx for ischemic stroke?
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
What is a transient ischemic attack?
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
Dural venous sinuses drain blood from cerebral veins and receive CSF from arachnoid granulations. What do they drain into?
internal jugular veins
pg 467
108
Where is CSF made?
by ependymal cells in the choroid plexus
109
Describe the path of CSF
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
Where does 4th ventricle CSF flow?
to the subarachnoid space via the:
foramine of Luschka (lateral)
foramen of Magendie (medial)
111
What is idiopathic intracranial HTN (pseudotumor cerebri)?
increased ICP with no apparnt cause on imaging (ie.. hydrocephalus, obstruction of CSF outflow)
112
How does a idiopathic intracranial HTN (pseudotumor cerebri) present?
with HA, diplopia (usually from CN VI palsy)
no mental status alcerations
papilledema seen on exam
113
What are the risk factors of idiopathic intracranial HTN (pseudotumor cerebri)?
woman of childbearing age
vitamin A excess
danazol
114
How is idiopathic intracranial HTN (pseudotumor cerebri) tx?
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
What is hydrocephalus?
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
What are the types of hydrocephalus?
- communicating (nonobstructive): communicating and normal pressure
- noncommunicating (obstructive)
117
What causes communicating hydrocephalus?
decreased CSF absorption by arachnoid granulation leading to increased ICP, papilledema, and herniation
118
What causes normal pressure hydrocephalus?
In the elderly, idiopathic in nature; CSF pressure elevated only episodically
does not result in increased subarachnoid space volume
119
How does normal pressure hydrocephalus present?
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
What causes a noncommunicating hydrocephalus?
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
What is ex vacuo ventriculomegaly?
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
What is Pick disease?
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
What is a classic finding of Pick disease?
A defining characteristic of the disease is build-up of tau proteins in neurons, accumulating into silver-staining, spherical aggregations known as "Pick bodies"
