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Neuro > Brain Exam 2 > Flashcards

Brain Exam 2 Flashcards

1
Q

Thalamus: origin and location

A
  • develops from diencephalon
  • located on either side of 3rd ventricle
  • supplied by proximal branches of PCA
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2
Q

Thalamus: function

A
  • relays info to cortex: receives input from subcortical structures
  • important for sensory motor integration
  • important for alert and conscious state
  • allows for modulation of signals before they enter cortex = selective attention
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3
Q

Internal medullary lamina

A
  • streaks of white matter that run through thalamus that form Y shape & divide thalamus
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4
Q

Medial geniculate body (MGB)

A
  • input: inferior colliculus

- cortex: auditory cortex (Heschl’s gyrus)

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5
Q

Lateral geniculate body (LGB)

A
  • input: optic tract

- cortex: visual cortex

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6
Q

Ventral posterior lateral nucleus (VPL)

A
  • input: dorsal column and spinothalamic tracts (body)

- cortex: somatosensory

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7
Q

Ventral posterior medial nucleus (VPM)

A
  • input: trigeminal (face)

- cortex: somatosensory

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8
Q

Ventral lateral geniculate body (VL)

A
  • input: cerebellum

- cortex: motor, premotor, supplementary motor

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9
Q

Ventral anterior geniculate body (VA)

A
  • input: basal ganglia

- cortex: motor, premotor, supplementary motor

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9
Q

Anterior nucleus

A
  • input: mammillary body, hippocampus

- cortex: cingulate gyrus

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10
Q

Dorsomedial nucleus (DM)

A
  • input: amygdala

- cortex: prefrontal cortex

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11
Q

Pulvinar nucleus

A
  • associated
  • input: parietal, temporal, occipital corticies
  • cortex: parietal, temporal, occipital corticies
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12
Q

Intralaminar nuclei

A
  • input: diverse sources including brain stem, reticular formation
  • cortex: diffuse (reticular activating system)
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13
Q

Pure sensory stroke

A
  • thalamic syndrome
  • lacunar infarct in VPL/VPM
  • often accompanied by small vessel disease assoc. w/ HTN and DM
  • typified by microatheroma and lipohyalinosis
  • loss of all sensation from body and face
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14
Q

Thalamic hemorrhage

A
  • spontaneous and usually assoc. w/ HTN
  • involvement of adjacent internal capsule dominates clinical picture
  • numbness and sensory deficits on contralateral side sometimes developing into thalamic pain
  • hemiparesis
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15
Q

Thalamic coma

A
  • infarcts in both reticular activating systems

- top of basilar artery occlusion

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16
Q

Hypothalamus: function

A
  • whole body homeostasis via regulation of ANS, endocrine system, and somatic motor activity (behavioral drives)
  • ensures survival of the individual and survival of the species
  • effects behaviors required to meet basic needs including feeding, drinking, reproduction
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17
Q

Circumventricular organs

A
  • select regions where BBB is interrupted allowing chemical communication between brain and systemic circulation
  • 3 in hypothalamus
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18
Q

Hypothalamic disturbances may result from

A
  • inflammation
  • tumors (intrinsic or extrinsic)
  • vascular disorders
  • hydrocephalus
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19
Q

Clinical disorders associated with hypothalamic lesions

A
  • hypothermia and hyperthermia
  • obesity and wasting
  • Diabetes Insipidus
  • disturbances of sleep
  • emotional disorders
  • hypogonadism and early puberty
  • altered growth patterns
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20
Q

The hypothalamus regulates the ANS through descending connections with the ____ and ____. Sites associated with ____ function tend to be located in anterior and ____ function in posterior.

A
  • brainstem
  • spinal cord
  • parasympathetic
  • sympathetic
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21
Q

Magnocellular system

A
  • neural; posterior lobe of hypothalamus
  • made of paraventricular (PVN) and supraoptic (SON) nuclei
  • synthesizes oxytocin [milk letdown] and vasopressin [water resorption] and transports to posterior pituitary for release
  • large diameter neurons
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22
Q

Parvicellular system

A
  • humoral; anterior lobe of hypothalamus
  • secretes releasing and inhibiting factors that regulate secretion from anterior pituitary via hypophyseal portal vessels
  • small diameter neurons
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23
Q

Major hypothalamic substances that stimulate or inhibit release of anterior pituitary hormones

A
  • GnRH -> FSH and LH
  • GHRH -> growth hormone
  • SS -| growth hormone
  • TRH -> TSH
  • DA -| prolactin
  • CRH -> ACTH
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24
Q

Hypothalamus: food intake and metabolism nuclei

A
  • ventromedial hypothalamus (VMH) [satiety center]
  • lateral hypothalamus (LH) [feeding center]
  • arcuate nucleus (ARC)
  • paraventricular nucleus (PVN)
  • dorsomedial nucleus (DMH)
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25
Q

Hypothalamus: day-night rhythms nuclei

A
  • suprachiasmatic nucleus (SCN)
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26
Q

Hypothalamus: temperature regulation nucleus

A
  • anterior hypothalamus (AH)
  • preoptic area (POA) [heat dissipation]
  • posterior hypothalamus (PH) [heat conservation]
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27
Q

The input to the hypothalamus to control the physiological manifestation of emotion comes from ____.

A
  • limbic structures
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28
Q

Limbic lobe

A
  • forms rim of cortex at junction between diencephalon and cerebral cortex
  • includes Papez circuit (hippocampus, fornix, mammillary bodies, anterior nucleus of thalamus, and cingulate gyrus)
  • and orbital and medial prefrontal cortex, amygdala, septal nuclei, dorsomedial nucleus of the thalamus, ventral striatum, hypothalamus
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29
Q

Hippocampus subsystem

A
  • has primarily an indirect role in emotion
  • essential for factual or declarative memory
  • specifically involved in consolidation process that requires sleep
  • bilateral damage results in profound anterograde amnesia
  • 3 layer cortex: dentate gyrus, hippocampus proper, subiculum
  • one way info flow: though dentate gyrus, CA3, CA2, CA1, to entorhinal cortex
  • CA1 sensitive to anoxia
  • impacted by chronic stress (a little stress enhances)
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30
Q

Amygdala

A
  • central to emotion and participates in acquisition, consolidation, and recall of emotional memory, aggression
  • important for determining affective perception of sensory stimuli: good or bad
  • plays central role in fear and fear conditioning
  • attaches emotional significance to various stimuli perceived by assoc cortex
  • 3 subnuclei: medial, basolateral, and central
  • 2 pathways: through sensory cortex or skip
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31
Q

Habituation

A
  • decreasing response to a sensory stimulus

- molecular basis: repeated stimulation causes depletion of glutamate vesicles at atonal terminal = less depolarization

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32
Q

Sensitization

A
  • increasing response to a sensory stimulus
  • molecular basis: interneuron releases serotonin, activating sensory neuron receptors. cAMP activates PKA -> more Ca influx = increased glutamate release
  • short term and long term
  • long term requires protein phosphorylation and protein synthesis
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33
Q

Associative conditioning

A
  • associating 2 sensory stimuli
  • aka Pavlovian conditioning
  • leads to formation of an associative memory
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34
Q

Early LTP molecular mech

A
  • increase in Ca
  • activation of protein kinases
  • phosphorylation of receptors
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35
Q

Late LTP molecular mech

A
  • increase in Ca
  • activation or protein kinases
  • phosphorylation of CREB
  • increased gene expression and protein synthesis
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36
Q

Learning and memory requires changes in ____.

A
  • synaptic strength
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37
Q

Short-term memory depends on ____ but not ____. ____ depends on both.

A
  • protein phosphorylation
  • protein synthesis
  • long-term memory
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38
Q

____ are essential for associative conditioning.

A
  • NMDA receptors
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39
Q

Frontal lobe functions

A
  • cognition, executive function, motor strip, execution of movement, frontal eyefields, Broca’s (dominant hemisphere) essential for spoken word, working memory
  • lesions: nonfluent aphasia
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40
Q

Parietal lobe functions

A
  • integrate sensory info, contains primary sensory strip, reading and math functions
  • lesions: contralateral neglect; Gerstman’s syndrome
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41
Q

Temporal lobe functions

A
  • auditory perceptions, primary auditory cortex, Wernicke’s essential for understanding speech, hippocampus and amygdala
  • lesion: fluent aphasia-dominant hemisphere
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42
Q

Cortex cellular organization

A
  • 6 layers
    I molecular layer: relatively free of cells; mostly axons
    II external granule layer: small cell bodies (sensory)
    III external pyramidal layer: big cell bodies (motor)
    IV internal granule layer
    V internal pyramidal layer
    VI polymorphic layer: mix of things
  • not uniform throughout cortex
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43
Q

Occipital lobe functions

A
  • processing and integrating visual information, primary & association visual cortex
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44
Q

Cortical connectivity: input to cortex

A
  • thalamic sensory and relay nuclei: layer IV
  • intrathalamic nuclei: layer VI
  • intracortical input (corpus callosum): layers II and III
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45
Q

Cortical connectivity: output from cortex

A
  • layer III: other cortical areas
  • layer V: striatum, brainstem, spinal cord
  • layer VI: thalamus
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46
Q

Association fibers vs. commissural fibers

A
  • association: stay w/in same hemisphere (superior longitudinal fasciculus, arcuate fasciculus, cinculum)
  • commissural: project from one hemisphere to the other (corpus callosum)
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47
Q

blood supply: MCA

A
  • primary motor
  • primary sensory
  • frontal eye fields
  • association sensory
  • Broca’s and Wernicke’s
  • supramarginal and angular
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48
Q

Blood supply: ACA

A
  • paracentral lobule

- cingulate gyrus

49
Q

Blood supply: PCA

A
  • visual cortex

- visual association cortex

50
Q

Retina cell layers

A
  • ganglion cells
  • bipolar cells
  • photoreceptors cells: stacks of discs of membranes that generate electrical signals from light absorption
51
Q

Rods vs. cones

A
  • black and white vs. color
  • blunt tip vs. tapered tip
  • more vs. less
  • none in fovea (concentrated around) vs. throughout retina and concentrated in fovea
  • dimly-lit vs. well-lit
  • many receptors vs. few receptors
  • poor acuity vs. excellent acuity
  • excellent sensitivity vs. poor acuity
52
Q

Visual cortex organization

A
  • forward and medial regions: motion and spatial relations (where)
  • lateral regions: form and color (what)
  • cuneus (upper) processes lower visual field
  • lingula (lower) processes upper visual field
53
Q

Fovea vs. peripheral retina

A
  • high vs. low threshold
  • cones only vs. rods and cones
  • limited or no convergence vs. extensive convergence
  • photopic vs. scotopic illumination
  • central, color, detail vision vs. peripheral, achromatic, poor detail vision
54
Q

Age Related Macular Degeneration

A
  • early stage: no symptoms
  • middle stage: blurred central vision, straight lines appear distorted and wavy, blurred or dark spot in center of vision gradually gets larger
  • later stages: patient might not recognize faces
  • does not typically affect peripheral vision or cause complete blindness
  • dry stages: drusen deposits and retinal pigment epithelium cells and neighboring photoreceptors degenerate
  • wet stages: new vessels invade subretinal space and they leak blood and plasma causing more degeneration
55
Q

Retinitis Pigmentosa

A
  • usually in younger people (genetic disease)
  • symptoms: decreased vision in low light, loss of peripheral vision causing tunnel vision, loss of central vision in advanced cases
  • slow progression; complete blindness uncommon
56
Q

Diabetic Retinopathy

A
  • symptoms: blurred vision, gradual vision loss, floaters, shadows or missing areas of vision, difficulty seeing at nighttime, cotton wool spots
  • usually none until damage is severe
  • nonproliferative stage: microaneurysms and retinal hemorrhages cause fluid leakage
  • proliferating stage: new fragile blood vessels form and hemorrhage; small scars develop; vision loss
57
Q

Glaucoma

A
  • leading cause of blindness worldwide
  • caused by buildup of pressure leading to damage of optic nerve head
  • open angle (majority), closed angle (emergency), and congenital (children)
  • open angle symptoms: none until damage severe; slow loss of peripheral vision that can lead to blindness
  • closed angle symptoms: sudden/severe pain in one eye, decreased or cloudy vision, nausea and vomiting, rainbow halos around lights, red eye
58
Q

If neither pupil constricts, suspect ____. If only one pupil constricts, suspect ____. If discrete area missing in one eye with no affront pupillary defect, suspect ____.

A
  • optic nerve involvement
  • oculomotor involvement
  • lesion on retina
59
Q

Motor neuron lesion locations

A
  • CNS (cerebral cortex, subcortex, brainstem, spinal cord)
  • anterior horn cell
  • peripheral nerve
  • neuromuscular junction
  • muscle
60
Q

UMN weakness

A
  • increased tone (spasticity)
  • increased deep tendon reflex; clonus
  • upper extremities tend to be flexed; lower extremities tend to be extended
  • Babinski sign present
  • less atrophy
61
Q

LMN weakness

A
  • decreased tone (flaccidity)
  • decreased deep tendon reflexes
  • fasciculations
  • Babinski sign absent
  • more atrophy
62
Q

Sensory lesion locations

A
  • CNS (cerebral cortex, subcortex, brainstem, spinal cord)

- peripheral nerve

63
Q

Peripheral sensory etiologies

A
  • symmetric “stocking glove” distribution (neuropathy) or

- fits individual nerve or root pattern

64
Q

Central sensory etiologies

A
  • spinal sensory level?
  • loss of touch/vibration on one side and pain/temp on other side?
  • hemisensory loss with face, arm, and leg?
65
Q

Altered mental status/cognition lesion location

A
  • CNS (cerebral cortex, subcortex, brainstem)
66
Q

Prosopagnosia

A
  • inability to identify faces

- bottom of temporal and occipital lobes on both sides of cortex

67
Q

Frontal lobe syndrome

A
  • behavioral changes: lack of responsibility/insight, indifference; abulia (slowed response to environment); hyper sexuality, incontinence, emotional lability
  • frontal release signs: suck, snout, palmomental, grasp reflexes; Gegenhalten (variable resistance to passive limb movement)
68
Q

Parietal lobe syndromes

A
  • visuospatial deficits
  • sensory integration: agraphesthesia, astereognosis, neglect
  • visual field deficit: pie in the floor
69
Q

Gerstmann syndrome

A
  • dominant parietal lobe syndrome
  • finger agnosia
  • acalculia
  • left-right confusion
  • agraphia
70
Q

Non-dominant parietal lobe syndrome

A
  • denial of deficit (anosognosia)
  • spatial difficulty (drawing, assembling blocks; hemineglect [almost always left side])
  • extinction on double-simultaneous stimuli
71
Q

Occipital lobe syndromes

A
  • contralateral homonymous hemianopia
  • cortical blindness: Anton’s syndrome (denial of blindness) and Balint’s syndrome (bilateral occipitoparietal; simultagnosia, optic ataxia, oculomotor apraxia)
72
Q

Temporal lobe symptoms

A
  • auditory integration
  • memory disturbance (bilateral hippocampus)
  • visual field deficit (Meyer’s loop - pie in the sky)
  • Wernicke’s aphasia
73
Q

ICA

A
  • internal carotid artery; large vessel
  • contralateral weakness
  • ipsilateral monocular vision loss (amaurosis fugax)
74
Q

ACA

A
  • anterior cerebral artery; large vessel
  • leg more than arms weakness/sensory deficit
  • language spared
75
Q

MCA

A
  • middle cerebral artery; large vessel
  • arm more than leg weakness; sensory deficit
  • aphasia on left, dysprosody on right
  • contralateral homonymous hemianopia/quadrantanopia
  • gaze deviation towards side of lesion
76
Q

PCA

A
  • posterior cerebral artery
  • contralateral homonymous hemianopia
  • alexia without agraphia (left PCA involving splenium)
77
Q

Pure motor hemiplegia

A
  • lacunar syndrome; assoc. w/ chronic HTN/lipohyalinosis

- internal capsule or ventral pons

78
Q

Pure hemisensory loss

A
  • lacunar syndrome; assoc. w/ chronic HTN/lipohyalinosis

- thalamus

79
Q

Sensorimotor loss

A
  • lacunar syndrome; assoc. w/ chronic HTN/lipohyalinosis

- thalamocapsular

80
Q

Clumsy hand dysarthria

A
  • lacunar syndrome; assoc. w/ chronic HTN/lipohyalinosis

- internal capsule, ventral pons, or corona radiata

81
Q

Ataxia hemiparesis

A
  • lacunar syndrome; assoc. w/ chronic HTN/lipohyalinosis

- ventral pons or internal capsule

82
Q

Watershed strokes

A
  • Acute hypoperfusion (i.e. cardiac arrest, vascular stenosis)
  • ischemia in distal areas of vascular supply: ACA-MCA -> proximal > distal weakness in arm and leg; MCA-PCA -> visuospatial deficits (Balint’s)
83
Q

Acute management of stroke

A
  • head CT
  • MRI brain with MRA head and neck
  • cardiac evaluation
  • check for diabetes, cholesterol
  • tPA if within 4.5 hours, thrombectomy
84
Q

Long term stroke management

A
  • antiplatelet agent
  • anticoagulation if indicated
  • statin
  • risk factor modification
85
Q

Intracerebral hemorrhage

A
  • causes: HTN**, AVM, tumor, amyloid angiopathy, hemorrhagic conversion of ischemic stroke
  • location: basal ganglia > pons > thalamus > cerebellum
  • may have sudden onset w/ smooth progression of deficit
86
Q

Aneurysms

A
  • outpouching due to weakness of vessel wall
  • occur at bifurcation
  • rupture leads to subarachnoid hemorrhage
87
Q

Subarachnoid hemorrhage

A
  • sudden onset terrible headache, stiff neck, photophobia, nausea/vomiting, transient LOC
  • spectrum of classification (1 to 5)
88
Q

Epilepsy

A
  • at least 2 unprovoked seizures; tendency to recurrent, unprovoked seizures
89
Q

Focal seizure

A
  • aka partial
  • simple: focal seizure w/ no impaired consciousness
  • complex: dyscognitive; impairment of consciousness
  • more likely to have a focal lesion
90
Q

Generalized seizure

A
  • refers to onset
  • spasm affects both sides of body almost contemporaneously
  • absence (petit mal): staring and lack of awareness; generalized spike and wave EEG
  • myoclonic
  • generalized clonic, tonic, tonic-clonic (grand mal): body stiffening and rhythmic activity
  • causes: genetic; metabolic derangement
91
Q

Brain tumor classification

A
  • intra-axial: in brain substance
  • gliomas: astrocytoma/glioblastoma multiforme, epemdymoma, oligodendroglioma
  • neuronal tumors: DNET;favors temporal lobe; seizures
  • metastasis
  • extra-axial: from outside brain
  • meningioma
  • schwannoma (acoustic neuroma)
  • neurofibroma
  • sella masses (pituitary adenoma, craniopharygioma)
  • metastasis
92
Q

Gliomas

A
  • astrocytoma: pilocytic (pediatric, benign, usually cerebellar); diffuse [low grade] (malignant but good prognosis, no enhancement); anaplastic (malignant, poor prognosis); glioblastoma multiforme (worst prognosis, most common glioma, likes to cross corpus callosum, pseudopallisading necrosis)
  • ependymoma: originates in ventricles, hydrocephalus common, low grade and slow growing
  • oligodendroglioma: slow-growing, good prognosis, “fried egg” histology, seizures common
93
Q

Meningiomas

A
  • extra-axial
  • signs due to compression
  • can be removed
  • slow-growing
  • good prognosis
94
Q

Stellar masses

A
  • extra-axial
  • headaches, bitemporal hemianopia
  • pituitary adenoma (hormonal symptoms)
  • craniopharyngioma (cystic)
95
Q

The ectoderm becomes the ____ (induction), which becomes the ____ (neurulation), which forms the ____.

A
  • neural plate
  • neural tube
  • CNS
96
Q

Failure of cranial neuropore closure results in ____. Failure of caudal neuropore closure results in ____. What else are neural defects associated with?

A
  • anencephaly
  • spina bifida
  • folate deficiency
97
Q

The neural crest forms ____.

A
  • PNS, ANS, & many more tissues

- in conjunction w/ mesoderm, it contributes to calvarium and meninges of brain

98
Q

Vesicles formation

A
  • prosencephalon -> telencephalon (cerebral hemispheres) and diencephalon (thalamus, hypothalamus, optic nerves)
  • mesencephalon -> midbrain
  • rhombencephalon -> metencephalon (pons, cerebellum) and myelencephalon (medulla)
99
Q

Malformations of cortical development

  • neuronal and glial proliferation -> ____.
  • neuronal cortical organization -> ____.
  • neuronal migration -> ____.
A
  • lissencephaly: abnormal decrease in cell proliferation; less gyri
  • polymicrogyria: cortex too thick; increased gyri
  • heterotopias: gray matter did not migrate out properly
100
Q

MS classification

A
  • relapsing-remitting: reverts back to baseline between attacks; inflammation
  • relapsing-progressive: reverts not quite back to baseline between attacks; inflammation; neurodegenerative
  • secondary progressive: coverts to a progressive course; neurodegenerative
  • primary progressive: progressive course from onset; neurodegenerative
101
Q

MS evaluation

A
  • demonstrate lesions in space and time: brain and spine MRI; clinical symptoms
  • evoked potentials (electrical testing)
  • lumbar puncture: >2 oligoclonal bands, increased IgG synthesis/IgG index, WBCs < 50
102
Q

Types of dementia

A
  • Alzheimer’s: loss of memory, executive function, visuospatial impairment, language, behavior
  • Lewy body: hallucinations, psychosis
  • vascular: stepwise progression of cognitive decline
  • frontotemporal: social disinhibition, abulia
103
Q

Alzheimer’s pathology

A
  • senile plaques: beta-amyloid

- neurofibrillary tangles: Tau protein

104
Q

Alzheimer’s disease types

A
  • unknown: ApoeE-4, age, female, head trauma
  • down’s syndrome
  • familial: early onset; autosomal dominant (APP, presenillin 1)
105
Q

Concussion

A
  • altered awareness/consciousness without gross injury
  • acute symptoms are transient (< 6 hrs)
  • post-concussion syndrome: residual symptoms lasting weeks to months or longer; headache, dizziness, fatigue, mild cognitive symptoms, mood changes
106
Q

Hematoma: epidural

A
  • middle meninges artery rupture
  • between dura and skull
  • skull fracture
  • lucid interval
  • biconvex
107
Q

Hematoma: subdural

A
  • rupture of bridging veins
  • between dura and brain
  • can be both acute and chronic
  • involved trauma can be mild (especially in elderly)
  • lens shape
108
Q

Coup injury

A
  • site of impact is directly over contusion
109
Q

Countrecoup injury

A
  • site of impact is on opposite side of head
110
Q

Classification of consciousness

A
  • alert
  • somnolence: state of drowsiness or near sleep
  • obtundation: mild to moderate reduction in alertness; accompanied by a lesser interest in environment
  • stupor: condition of deep sleep or similar behavioral unresponsiveness from which the subject can be aroused only with vigorous and continuous stimuli; responds to voice/pain
  • coma: both arousal and awareness are severely depressed (> 1 hr); cortical and subcortical (no eye movement)
  • encephalopathy: syndrome of global brain dysfunction
111
Q

Coma causes

A
  • compressive: cerebral (bilateral subdural hematoma); diencephalon (thalamus hemorrhage, hypothalamus tumor); brainstem (uncial herniation, cerebellum)
  • destructive: cerebral hemisphere (cortex [acute anoxia], subcortical [delayed anoxia], diencephalon [bilateral thalamic injury/stroke], brainstem [midbrain, pons stroke])
112
Q

Persistent vegetative state

A
  • patient may open eyes, but no interaction with environment
  • brainstem is working, but cortex is not
  • diagnosis after 1 month; 1 year in trauma cases
113
Q

Minimally conscious state

A
  • between PVS and normal
  • can follow simple commands
  • may gesture or verbalize yes/no responses
  • may have intelligible verbalization
  • demonstrates purposeful behavior rather than reflexive
114
Q

Locked-in syndrome

A
  • patient is awake but incapable of movement and speech
  • eye movements possible
  • ventral pontine lesion
  • respiration can be normal due to sparing of chemoreceptors in ventral medulla
115
Q

Glasgow coma scale

A
  • eye opening (1-4): 1 = no response, 2 = noxious stimulus, 3 = voice, 4 = normal
  • verbal response (1-5): 1 = no response, 2 = incomprehensible; 3 = inappropriate words, 4 = confused, 5 = normal
  • motor response (1-6): 1 = no response, 2 = extensor, 3 = flexor, 4 = withdraws to noxious stimulus, 5 = localized to pain only, 6 = normal
  • 8 or less is serious head injury
117
Q

Management of ICP

A
  • elevate head
  • hyperventilation
  • osmotic diuretics
  • barbiturate coma
  • CSF drainage (ventriculostomy)
  • hemicraniectomy
118
Q

cortical lesion

A
  • behavioral/personality changes
  • language disorder
  • visual field deficit
  • higher cortical sensory deficit
  • apraxia
  • neglect
  • hemiparesis (part of side)
  • hemiesthesia (part of side)
  • seizure
119
Q

subcortical lesion

A
  • pure motor deficits (may be whole side)
  • pure sensory deficits (may be whole side)
  • movement disorders
  • absence of cortical deficits
120
Q

brainstem lesion

A
  • crossed signs
  • CN deficit
  • vestibular, visual field deficits
  • cerebellar signs
  • could be bilateral signs
121
Q

spinal cord lesion

A
  • usually bilateral motor/sensory
  • no involvement above neck
  • UMN/LMN combo
  • bowel/bladder dysfunction
  • autonomic dysfunction

Neuro (3 decks)

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