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Nervous System: Unit IV > Cumulative Review > Flashcards

Cumulative Review Flashcards

1
Q

[Synaptic transmission] Mechanism of NT release at the presynaptic cell

A
  • AP reaches the end of the cell (“active zone”)
    • Active zone ECa = +120mV b/c the concentration of Ca2+ is significantly higher outside the cell
  • Ca2+ channels open ==> Ca2+ flows in quickly
  • Ca2+ attaches to vesicles containing NTs via SNARE proteins ==> fusion of vesicle to cell
  • NTs escape into the synaptic cleft
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2
Q

[Synaptic transmission} Mechanism of SNARE-mediated vesicle fusion

A
  • Ca2+ attaches to synaptotagmin (located on vesicle)
  • Synaptobrevin, syntaxin, and SNAP-25 form a super-helix used to fuse with the membrane
  • Vesicle fuses with membrane and NTs are released into the synaptic cleft
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3
Q

[Synaptic transmission} Major function of motor nerve terminal

A
  • AP from CNS ==> enough ACh to depolarize muscle fiber to threshold for AP
  • Muscle fiber resting = -80mV & threshold = -50mV ==> enough ACh to depolarize muscle by at least 30mV
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4
Q

[Synaptic transmission} Myasthenic syndrome characteristics

A
  • Ab againsts Ca2+ channels
  • Characteristically weak, but can fire APs @ muscle & improve strength with effort
    • relies on facilitation to build up enough Ca2+ to release enough NTs to generate APs @ muscle
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5
Q

[Synaptic transmission} Myasthenia gravis characteristics

A
  • Disease w/Abs against AChR ==> initial strength is good, but tire very quickly
    • With fewer postsynaptic AChR, M.G. people generally need to release more quanta to fire APs
    • Due to synaptic depression (reduction of 10% of available quanta/AP), M.G. people quickly fall below the required number of quanta to fire APs @ muscle
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6
Q

[Anterior Horn/Peripheral/NMJ Disorders] Signs/symptoms of upper motor neuron disorders

A
  • spastic tone
  • hyperactive tendon reflexes
    • pathologic reflexes (Babinski)
  • emotional lability (inappropriate laughing and crying)
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7
Q

[Anterior Horn/Peripheral/NMJ Disorders] Signs/symptoms of lower motor neuron disorders

A
  • muscle atrophy
  • fasciculation
  • diminished tone (flaccidity)
  • reduced or absent reflexes
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8
Q

[Anterior Horn/Peripheral/NMJ Disorders] Signs/symptoms of non-motor (sensory or autonomic) peripheral nerve disorders

A
  • sensory
    • numbness
    • pain
    • altered sensation
  • autonomic
    • bowel, bladder disturbance
    • altered sweating, HR, BP
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9
Q

[Anterior Horn/Peripheral/NMJ Disorders] Conditions w/rapidly developing muscle weakness

A
  • NMJ disorders
    • myasthenia gravis
    • botulism
    • organophosphate poisoning
  • acute demyelination
    • Guillain Barre
  • electrolyte disturbance
  • toxic myopathies
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10
Q

[Anterior Horn/Peripheral/NMJ Disorders] Anterior Horn cell disorders (examples)

A

Amyotrophic lateral sclerosis*

Spinal muscular atrophy

Poliomyelitis and West Nile virus

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11
Q

[Anterior Horn/Peripheral/NMJ Disorders] Peripheral neuropathies (polyneuropathy examples)

A

Hereditary – Charcot Marie Tooth disease*

Systemic disease – diabetes*, immune disorders etc

Vitamin deficiency – B12 deficiency, etc.

Exogenous toxins – alcohol, chemotherapy, etc.

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12
Q

[Anterior Horn/Peripheral/NMJ Disorders] NMJ disorders

A

Myasthenia gravis*

Botulism

Organophosphate poisoning

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13
Q

[Anterior Horn/Peripheral/NMJ Disorders] Myopathies examples

A

Muscular dystrophies – Duchenne/Becker*

Myotonic disorders

Inflammatory myopathies – polymyosits, dermatomyositis

Metabolic myopathies – glycogen storage, lipid myopathy

Endocrine/toxic myopathies

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14
Q

[Anterior Horn/Peripheral/NMJ Disorders] ALS signs/symptoms

A
  • progressive weakness & wasting
  • coexisting: spasticity & hyperreflexia
  • asymmetric limb weakness + fasciculations
  • foot drop or hand deformity possible
  • speech may be slurred/spastic
  • diaphragm weakness ==> decreased breathing capacity + impaired swalling ==> aspiration pneumo or respiratory insufficiency
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15
Q

[Anterior Horn/Peripheral/NMJ Disorders] Most common type of diabetic neuropathy + presentation

A
  • distal sensory or sensorimotor polyneuropathy
  • initial numbness and burning dysesthesias in feet ==> legs & hands
  • weakness of foot dorsiflexor ==> foot drop gait
  • diminished grip strength/hand dexterity
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16
Q

[Anterior Horn/Peripheral/NMJ Disorders] Sensation in diabetic neuropathy

A
  • loss of pin sensation in stocking glove distribution (often asymmetric)
  • “Large fiber pattern”
    • loss of position, vibration and light touch
    • decreased reflexes
  • “Small fiber injury”
    • prounounced loss of pain and temperature sensation
    • w/pain (dull aching; distal burning @ night)
    • NCVs may be near normal
  • autonomic dysfunction
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17
Q

[Anterior Horn/Peripheral/NMJ Disorders] Myasthenia Gravis presentation (signs/symptoms)

A
  • fluctuating weakness & fatigue @ cranial, limb, or trunk musculature
  • ocular sx: ptosis, diplopia and blurred vision
  • weak facial muscles ==> slurred/nasal/hoarse speech
    • ==> trouble chewing/swallowing
  • weak respiratory muscles ==> SOB
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18
Q

[CNS Injury] Types of forces resulting in cerebral trauma

A
  • contact phenomena
  • acceleration
    • translational
    • rotation
  • penetrating
  • secondary injury
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19
Q

[CNS Injury] Layers of Scalp

A
  • S = skin
  • C = subcutaneous tissue
  • A = galea
  • L = loose connective tissue
  • P = periosteum
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20
Q

[CNS Injury] Contact phenomena head injuries cause & effects

A
  • result from an object striking the head
  • ==> lacerations of the scalp
  • ==> fractures of skull
  • ==> epidural hematomas
  • ==> cerebral contusions
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21
Q

[CNS Injury] Skull fracture types

A
  • contact phenomenon to skull
  • types: linear, depressed, basilar, diastatic, and growing
    • linear = indicates high-impact injury
    • depressed = comminuted bone fragments
    • basilar = base of skull ==> CSF leaks ==> meningitis
    • diastatic = separates at suture lines
    • growing = infancy; from dural tears
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22
Q

[CNS Injury] Concussion definition

A
  • =”mild traumatic brain injury”
  • = laternation in mental status, distrubance of equilibrium caused by biomechanical forces which may/may not lead to loss of consciousness
  • hallmarks = confusion & amnesia
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23
Q

[CNS Injury] Common concussion symptoms

A
  • headache
  • dizziness
  • poor attention, inability to concentrate
  • fatigue, sleep disturbance
  • irritability, depressed mood
  • intolerance of bright light or loud noise
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24
Q

[CNS Injury] Types of acceleration injuries

A
  • transalational: head movement in single plane after impact
  • rotational: head movement in multiple planes
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25
Q

[CNS Injury] Signs of basilar skull fracture

A

•CSF rhinorrhoea •Bilateral periorbital haematomas (Racoon eyes) •Subconjunctival haemorrhage •Bleeding from external auditory meatus •CSF otorrhoea •Battle’s sign •Facial nerve palsy

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26
Q

[CNS Injury] Consequences of transalation acceleration injuries

A
  • stretching/tearing of veins between brain and dura ==> subdural hematoma
  • brain contusion
  • coup/contrecoup injuries
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27
Q

[CNS Injury] Characteristics of brain contusion

A
  • often due to transalational acceleration injuries
  • often occurs @ frontal/temporal
  • can lead to swelling, brain shift, increase in intracranial pressure, herniation
  • low mortality alone
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28
Q

[CNS Injury] Examples of rotational acceleration injuries

A
  • MVA ejection
  • motorcycle accident
  • auto-pedestrian accident
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29
Q

[CNS Injury] Consequences of rotational acceleration injury

A
  • ==> microscopic tearing of nerve cells @ brain
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30
Q

[CNS Injury] Characteristics of epidural hematomas

A
  • Caused by contact phenomena
  • extradural arterial hemorrhage
  • Associated with skull fractures
  • Classic “lucid interval” after trauma occurs
  • Low mortality rate
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31
Q

[CNS Injury] Characteristics of subdural hematoma

A
  • caused by translational acceleration injuries
  • rupture of bridging veins in subdural space
  • associated with brain contusions
  • high mortality rate
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32
Q

[CNS Injury] Characteristics of Coup/contrecoup injury

A
  • often caused by translational acceleration injury
  • brain contusions + shearing forces on brain/veins in both the rostral and caudal directions due to impact and rebound
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33
Q

[CNS Injury] Common consequences of rotational acceleration injury

A
  • diffuse axonal injury ==> microscopic tearing of nerve cells in brain
  • under a microscope = “axonal spheroids”
  • patients are usually in chronic vegetative state
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34
Q

[CNS Injury] Goal of treatment in head injuries

A
  • save any neurons that have reversible damage
  • minimize secondary effects/mitigate symptoms
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35
Q

[CNS Injury] Importance of controlling ICP

A
  • increased ICP ==> CSF in spinal subarachnoid space OR venoconstriction @ CNS capacitance vessels ==> blood displacement into jugular venous system
  • ==> herniation of brain (which is non-compressible) ==> brain damage
  • also: if ICP > MAP, then there will not be blood flow to brain ==> syncope & eventaully cell death
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36
Q

[CNS Injury] Common signs/symptoms of increased ICP

A
  • sudden change in neurological condition
  • headache, nausea, vomiting ==> progressive lethargy and LOC
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37
Q

[CNS Injury] Herniation syndromes (4)

A
  • subfalcine herniation
  • central herniation
  • uncal transtentorial herniation
  • tonsillar herniation
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38
Q

[CNS Injury] Characteristics of subfalcine herniation

A
  • cingulate gyrus is pushed away from the expanding mass and herniates beneath the falx cerebri.
  • The anterior cerebral artery is often kinked, which may result in a stroke in distribution of this vessel.
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39
Q

[CNS Injury] Characteristics of central herniation

A
  • Occurs when there is downward pressure centrally
  • can result in bilateral uncal herniation
  • results in loss of consciousness.
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40
Q

[CNS Injury] Characteristics of uncal transtentorial herniation

A
  • the uncus herniates across the tentorial edge, and downward into the posterior fossa
  • herniation compresses the midbrain and its ipsilateral cerebral peduncle
    • ==> ipsilateral third nerve palsy (test pupillary light reaction, could be fixed and dilated)
    • ==> contralateral hemiparesis (paralysis of one side of body)
  • Rarely, uncal herniation can compress the opposite cerebral peduncle against the tentorial edge, resulting in a hemiparesis that is ipsilateral to the mass lesion and herniated uncus.
41
Q

[CNS Injury] Characteristics of tonsillar herniation

A
  • cerebellar tonsils herniate downward into the foramen magnum (coning)
  • medulla is compressed → abnormal cardiac and respiratory responses, including Cushing’s reflex (bradycardia and hypertension) in the setting of high intracranial pressure.
  • Tonsillar herniation most commonly is encountered in the setting of a mass lesion in the posterior fossa.
42
Q

[CNS Injury] Critical avoidance in context of intracranial mass lesion

A
  • DO NOT PERFORM A LUMBAR PUNCTURE
  • lumbar punctures can precipate herniation syndromes due to pressure differentials created during the procedure
43
Q
A
44
Q

[Delirium/Dementia] Delirium DSM definition

A
  • disturbance in attention and awareness
  • disturbance develops over a short period of time
    • change from baseline attention
    • tends to fluctuate during course of day
  • additional cognitive disturbance
  • evidence that disturbance is a direct consequence of another medical condition
    • substance intoxication/withdrawal
    • toxin
    • multifactorial
45
Q

[Delirium/Dementia] Possible underlying causes of delirium

A
  • infection
  • electrolyte abnormalities
  • hypoglycemia
  • cardiac/pulmonary/hepatic/renal failure
  • endocrine
  • medications
  • drugs, withdrawal
  • trauma
  • epilepsy
46
Q

[Delirium/Dementia] Delirium mechanism

A
  • Disrupted ascending activation from reticular activating system and thalamus to the cortex
    • both very sensitive to metabolic stress
  • •Potentially involving multiple transmitter systems: dopamine, acetylcholine, norepinephrine, and serotonin
47
Q

[Delirium/Dementia] Management of delirium

A
  • •Low dose Haldol; IV form
  • •May use low dose atypicals if PO
  • •Donepezil
  • •Unless EtOH withdrawal, avoid pitfalls of benzos and paradoxical agitation
  • •Physical restraints only during acute agitation and promptly removed
48
Q

[Delirium/Dementia] Dementia DSM definition

A

A.Evidence of significant cognitive decline from a prior level of performance in one or more cognitive domains

B.Cognitive deficits interfere with independence in everyday activities

C.Do not occur exclusively in context of delirium

D.Not better explained by another mental disorder (i.e., depression, schizophrenia)

49
Q

[Delirium/Dementia] General characteristics of dementia

A
  • “top-down” cognitive fxnl impairment
    • i.e. isolated memory problems w/out attention issues
  • decline from previous baseline
  • changes in personality, mood, perception
  • numerous causes:
    • neurodegenrative: Alzheimers
    • vascular
    • obstructive
    • neoplastic
    • infectious
    • trauma
  • depression can present as dementia
50
Q
A
51
Q

[Neurodegenerative] General overview/underlying cause of neurodegenerative disorders

A
  • often due to spontaneous failure w/in body
  • includes spontaneous death of a neuronal population
    • location of population ==> clinical presentation
52
Q

[Neurodegenerative] Common dementia-related problems in neurodegenerative diseases

A
  • memory
  • language
  • executive function
  • visuospatial
  • depression, apathy, sociopathy
53
Q

[Neurodegenerative] Common movement disorder problems in neurodegenerative diseases

A
  • bradykinesia
  • rigidity
  • tremor
  • chorea = involuntary movement disorder
54
Q

[Neurodegenerative] Dementia could indicate…

A
  • Alzheimer’s disease
  • FTD
  • Lewy body
  • HD
  • CJD
55
Q

[Neurodegenerative] Movement disorders could indicate…

A
  • Parkinson’s
  • PSP (progressive supranuclear palsy)
  • CJD
  • Huntingtons
56
Q

[Neurodegenerative] Alzheimer’s disease: Clinical Features & Transmission

A
  • clinical = early memory and visuospatial problems
  • transmission
    • most = sporadic
    • genetic
      • presenilin 1 mutation
      • trisomy 21
57
Q

[Neurodegenerative] Parkinson’s disease: Clinical Features & Transmission

A
  • tremor, rigidity, bradykinesia
    • leads to slow speech and movement
  • genetic and sporadic transmission
58
Q

[Neurodegenerative] Lewy Body Dementia: Clinical Features & Transmission

A
  • early parkinsonian features, psychosis, fluctuating consciousness
  • genetic and sporadic transmission
59
Q

[Neurodegenerative] Huntington’s disease: Clinical Features & Transmission

A
  • dementia
  • depression, sociopathy (aggression)
  • chorea
  • inherited: autosomal dominant
60
Q

[Neurodegenerative] Alzheimer’s disease: Neurochemistry & Neuropathology

A
  • ACh deficit (cholinergic hypothesis)
  • Amyloid plaques and neurofibrillary tangles
  • diffuse atrophy globally
  • cortex and hippocampus involved
61
Q

[Neurodegenerative] Parkinson’s disease: Neurochemistry & Neuropathology

A
  • Chemistry
    • Synuclein
    • Dopamine deficit
  • Pathology
    • Lewy bodies
62
Q

[Neurodegenerative] Lewy Body Dementia: Neurochemistry & Neuropathology

A
  • ACh deficit
  • Dopamine deficit
  • Lewy bodies
63
Q

[Neurodegenerative] CJD: Neurochemistry & Neuropathology

A
  • prion protein
64
Q

[Neurodegenerative] Huntington’s disease: Neurochemistry & Neuropathology

A
  • polyglutamine
  • characteristic gross changes w/out microscopic changes
  • caudate nucleus atrophy
  • ventricles ==> butterflies
65
Q

[Neurodegenerative] Characteristics of prion diseases

A
  • can be sporadic, heritable, or transmissible/infectious
  • caused by proteinaceious infectious particle w/out nucleic acid
    • natural protein ==> deforms to beta pleated sheet
  • uniformly fatal diseases
66
Q

[Stroke} Presentiation of large vessel ischemic stroke/TIA

A
  • ==> deficits in multiple systems
  • e.g. @ middle cerebral ==> hemiparesis, hemisensory loss, defect in visual field contralateral to ischemic side of brain
67
Q

[Stroke} General presentation of small vessel ischemic stroke/TIA

A
  • ==> isolated motor or sensory deficit in one side of the body
68
Q

[Stroke} Common non-atherosclerotic causes of stroke in young patients

A
  • coagulopathy
  • sickle cell anemia
  • oral contraceptives, post partum
  • antiphospholipid ab syndrome
69
Q

[Stroke} Rescuscitation related to stroke mechanism

A
  • ischemic stroke
  • resuscitation ==> break up clot and maintain volume of blood to maintain brain perfusion
70
Q

[Stroke} Prevention related to stroke mechanism

A
  • keep arteries healthy ==> prevention of atherosclerosis and hypercoaguability
    *
71
Q

[Stroke} Basic principles /goals of emergency tx of stroke

A
  • preserve non-infarcted areas of brain
  • prevent progression of infarction
  • avoid complication
  • initiate evaluation for long-term therapy
72
Q

[Stroke} Tx of ischemic stroke @ ER

A
  • act fast even w/normal scans
    • If CT scan shows hemorrhage, then you know that it is hemorrhagic.
    • If not, you know it is ischemic when combined with the story and clinical signs.
  • Re-open arteries with a catheter, thrombolytics.
    • generally a 4 hour IV window for thrombolytics
    • Tissue Plasminogen Activator (TPA) is the drug of choice.
  • Keep fluids up, maximize cardiac output, and resist the temptation to lower blood pressure (unless dangerously high)
  • treat hypoglycemia when it exists.
73
Q

[Stroke} Fluids used in emergency ischemic stroke tx

A
  • Avoid lowering BP
    • most stroke patients have HTN following a stroke that fixes itself within 7-10 days
  • If they won’t decompensate into heart failure, you can give normal saline.
  • If they will, give d5W unless they are having a very large stroke and at risk for cerebral edema.
74
Q

[Stroke} Clinical presentation of ruptured intracranial aneurysm

A
  • sudden onset neurological deficits
  • headache
    • “worst headache of their life”
  • nausea, vomiting
  • depressed level of consciousness
75
Q

[Stroke} Clinical presentation of ruptured intracerebral hemorrhage

A
  • begins: mild headache, mild neuro deficits, some nausea ==(minutes - hours)==> + decreased level of consciousness
  • hemiparesis ==> hemiplegia
  • decreased consciousness ==> coma
76
Q

[Stroke} Clinical presentation of acute subdural hemorrhage

A
  • Due to trauma or spontaneous
  • confusion, lethargy, coma,
  • focal neurologic symptoms, seizures
  • headache, dizzines
  • N/V, ataxia
77
Q

[Stroke} Clinical presentation of epidural hemorrhage

A
  • trauma/injury ==> period of grogginess ==> lucid interval ==> worsening condition/consciousness
  • commonly = traumatic temporal bone fracture tears middle meningeal artery
78
Q

[Stroke} Emergency treatment of hemorrhage

A
  • if ischemic ==> hemorrhage then use anti-platelets/anticoagulants
  • rapid dx ==> ICP monitoring device +/- drainage device
  • reduce ICP via diuresis and reduction of blood pCO2
  • emergency surgery if neccessary
    • common in subdural and epidural hemorrhage
79
Q

[Toxic-metabolic] Clinical features of Wernicke’s encephalopathy

A
  • Thiamine deficiency (vitamin B1)
  • Wernicke’s encephalopathy - full triad of ataxia, nystagmus (or ophthalmoplegia) and confusion
    • these signs not always present
  • Korsakoff’s psychosis
  • Peripheral neuropathy
80
Q

[Toxic-metabolic] Etiology of Wernicke’s encephalopathy

A
  • Vitamin B1 (Thiamine) deficiency
  • Alcoholism = common cause
    • ==> poor food intake + reduced absorption
  • Patients w/GI or absorbing problems are also at risk
81
Q

[Toxic-metabolic] Radiographic finding in Wernicke’s encephalopathy

A
  • 50% of cases detectable by MRI
  • damage to affected structures (mammillary body, ventricles, etc.)
  • disruption of BBB
82
Q

[Toxic-metabolic] Characteristics of Korsakoff’s Psychosis

A
  • Memory loss associated with Wernicke’s encephalopathy
  • Thiamine deficiency ==> damage to dorsomedial nucleus
83
Q

[Toxic-metabolic] Etiology of Hepatic Encephalopthy

A
  • often: Alcoholism ==> cirrhosis ==> reduced liver fxn ==> increased toxins
  • Increased ammonia (from catabolism of proteins) ==> disturbance of amino acid balance ==> disturbance of inhibitory and excitatory NTs @ brain
84
Q

[Toxic-metabolic] Presentation of Hepatic Encephalopathy

A
  • Episodes of confusion, forgetfulness ==>
  • drowsiness, stupor ==>
  • coma
85
Q

[Toxic-metabolic] Etiology of Cobalamin deficiency

A
  • Vitamin B12 deficiency
  • causes:
    • reduced dietary intake (e.g. of meat/dairy)
    • pernicious anemia
      • inability to absorb B12
    • gastric neoplasms, gastrectromy
86
Q

[Toxic-metabolic] Clinical presentation of Cobalamin deficiency

A
  • Megaloblastic anemia (~70% of cases)
  • disorder of dorsal column + lateral corticospinal tract ==>
    • diminished vibration + proprioception of lower limbs
    • abnormal reflexes
    • spacsticity
    • incontinence
    • orthostatic hypotension
  • damage to cerebral hemispheric white matter ==>
    • psychoses
    • dementia
  • damage to optic nerve (rare)
    • visual changes
87
Q

[Toxic-metabolic] Treatment of Colbamin deficiency

A
  • parenteral administration of vitamin B12
88
Q

[Toxic-metabolic] Etiology/Presentation of Central Pontine Myelinolysis (CPM)

A
  • electrolyte imbalance resulting from rapid correction/overrcorrection of hyponatremia
    • low serum sodium ==> water into cells ==> cytotoxic edema
    • fluid restriction + hypertonic saline ==> overcorrection ==> high blood osmolarity ==> flow across BBB
  • Sx: confusion, delirium, balance issues, speech problems, difficulty swallowing
89
Q

[Toxic-metabolic] Etiology of Wilson’s Disease

A
  • Autosomal recessive
  • Chromosome 13 gene
  • disorder of copper metabolism
  • mean age of presentation = 12 years
    • may present w/signs of liver disease + motor/neuro signs
90
Q

[Cortical Lesions] Role of Frontal Lobe in human cognition

A
  • voluntary movement
  • language fluency (left)
  • motor prosody (right)
  • comportment
  • executive fxn
  • motivation
91
Q

[Cortical Lesions] Role of Parietal Lobe in human cognition

A
  • tactile sensation
  • visuospatial function (right)
  • attention (right)
  • reading (left)
  • writing (left)
  • calculation (left)
92
Q

[Cortical Lesions] Role of Temporal Lobe in human cognition

A
  • language comprehension (left)
  • sensory prosody (right)
  • memory
  • emotion
93
Q

[Cortical Lesions] Role of Occipital Lobe in human cognition

A
  • vision
  • visual perception
  • visual recognition
94
Q

[Cortical Lesions] Major frontal lobe syndromes

A
  • Broca’s aphasia
  • orbitofrontal lesions ==> disinhibition
  • dorsolateral preforntal lesions ==> executive dysfxn
  • medial frontal lesions ==> apathy
95
Q

[Cortical Lesions] Temporal lobe syndromes

A
  • Wernicke’s aphasia
  • sensory aprosody
  • amnesia
  • emotional disorders
96
Q

[Cortical Lesions] Characteristics of Wernicke’s aphasia

A
  • due to lesion @ posterior region of left superior temporal gyrus
  • auditory comprehension of language is impaired
97
Q

[Cortical Lesions] Characteristics of amnesia

A
  • due to hippocampal lesion
  • amnesia = new learning deficit = inability to encode new memories
98
Q

[Cortical Lesions] Characteristics of hemineglect

A
  • due to parietal lesions
  • = failure to report, respond to, or orient sensory stimuli
  • more common after right hemisphere lesions (dominant for attention) ==> inattention to one side of body or extrapersonal space
99
Q

Major occipital lobe syndromes

A
  • visual agnosia
  • visual field deficit

Nervous System: Unit IV (26 decks)

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