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Brain & Behavior Extras > Summative Pathologies > Flashcards

Summative Pathologies Flashcards

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1
Q

Alternating Hemiplegia

A

Clinical Presentation: contralateral body deficits: spastic paralysis, weakness, loss of touch and proprioception; Ipsilateral facial deficits
MOA: Midline lesions of the brainstem

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2
Q

Berry Aneurysm

A

Clinical Presentation: Sudden onset of double vision and severe headache; incomplete adduction and elevation of the eye on affected side
MOA: saccular or intracranial aneurysm
*most common cause of subarachnoid hemorrhage

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3
Q

Lateral Medullary Syndrome

A

Clinical Presentation: Ipsilateral - palatal weakness and numbness, facial numbness, Horner’s syndrome and vertigo; Contralateral loss of pain and temperature; ataxia, and dysphagia
MOA: ischemia in the lateral part of the medulla; often due to damage to PICA

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4
Q

Bulbar Palsy

A

Clinical Presentation: Dysphagia, difficulty chewing, slurring of speech ,dystonia, dysarthria
MOA: LMN lesion in the medulla or outside the brain stem
*pseudobulbar palsy has the same presentation but is due to UMN damage of corticobulbar tracts in mid pons

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5
Q

Abducens Ophthalmoplegia

A

Clinical Presentation: Diplopia; affected eye deviates medially at rest and can’t abduct during lateral gaze
MOA: Paralysis of lateral rectus muscle

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6
Q

Trochlear Ophthlamoplegia

A

Clinical Presentation: Affected eye extorts; can’t intort eye; patient tilts head away from lesion
MOA: Trochlear nerve damage

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7
Q

Oculomotor Ophthalmoplegia

A

Clinical Presentation: Abduction of affected eye, ptosis, mydriasis
MOA: Oculomotor lesion/damage; disrupts PSYM innervation of pupil

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8
Q

Internuclear Ophthalmoplegia

A

Clinical Presentation: Ipsilateral can’t follow contralateral eye when gaze is to contralateral side; nystagmus in the contralateral eye
MOA: Damage to MLF (medial longitudinal fasiculus) which communicates among oculomotor nuclei
Ex: Lesion to L MLF will cause L oculomotor paralysis and L beating nystagmus when looking R

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9
Q

Medial Medullary Syndrome

A

Clinical Presentation: Contralateral loss of touch, vibration, and proprioception; contralateral spastic hemiplegia in arm and leg; ipsilateral flaccid paralysis of tongue
MOA: damage to anterior spinal artery which perfuses the medial medulla

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10
Q

Medial Pontine Syndrome

A

Clinical Presentation: Contralateral loss of touch, vibration, and proprioception; contralateral spastic hemiplegia in arm and leg; ipsilateral abducens ophthalmoplegia
MOA: Damage to paramedian branches of the basilar artery which perfuses the medial pons

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11
Q

Lateral Pontine Syndrome

A

Clinical Presentation: Loss of contralateral pain and temperature sensation; loss of ipsilateral face pain and temperature sensation; ipsilateral Horner’s; ataxia, unsteady gait, fall toward side of lesion; vertigo, nausea, nystagmus, deafness, tinnitus, vomiting; ipsilateral paralysis of masticatory muscles
MOA: Damage to long circumferential branch of basilar artery which perfuses lateral pons

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12
Q

Medial Midbrain Syndrome

A

Clinical Presentation: Contralateral loss of touch, vibration, and proprioception; contralateral spastic hemiplegia in arm and leg; UMN paralysis of contralateral lower face and contralateral deviation of tongue protrusion. Ipsilateral ophthalmoplegia with fixed and dilated pupil
MOA: Damage to paramedian branches of the basilar bifurcation and P1 segment of PCA which perfuses the medial midbrain

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13
Q

Posterior Cerebral P1 Syndrome

A

Clinical Presentation: Upper alternating hemiplegia, thalamic syndrome
MOA: Damage to P1 segment of PCA

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14
Q

Thalamic Syndrome

A

Clinical Presentation: Contralateral hemisensory loss; burning pain in the affected areas, hemiparesis, hemiballismus, choreoathetosis, intention tremor, ataxia
MOA: Damage to thalamogeniculate artery, loss of blood supply to VPM and VPL

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15
Q

Werdnig-Hoffman Disease

A

Clinical Presentation: Severe and diffuse weakness, poor feeding, respiratory insufficiency; sparing of facial and oculomotor muscles; reduced or absent deep tendon reflexes
MOA: AR inherited degeneration of the anterior motor horn
*death occurs within a few years after birth; 85% by 17 months

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16
Q

Amyotrophic Lateral Sclerosis (ALS)

A

Clinical Presentation:
Lower signs- flaccid paralysis with muscle atrophy, fasciculations, weakness with decreased muscle tone, impaired reflexes, negative Babinski sign
Upper signs - spastic paralysis with hyperreflexia, increased muscle tone, positive Babinski sign
MOA: Degeneration of upper and lower motor neurons of the corticospinal tract; anterior motor horn degeneration leads to lower motor neuron signs; lateral corticospinal tract degeneration leads to upper motor neuron signs
Labs: TDP-43 protein aggregates in motor neurons, corticospinal tract degeneration
*SOD1 (superoxide dismutase) mutation present in some familial cases (leads to free radical injury in neurons); atrophy and weakness of hands is early sign

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17
Q

Parkinson Disease

A

Clinical Presentation: TRAP - Tremor at rest, Rigidity in extremities Akinesia/bradykinesia, Postural instability and shuffling gait
MOA: Loss of dopaminergic neurons in the substantia nigra of the basal ganglia; related to aging; unknown etiology
Histo: loss of pigmented neurons in substantia nigra and round eosinophilic inclusions of alpha-synuclein (Lewy bodies)
Tx: L-dopa (administer with carbidopa to minimize peripheral conversion); pallidotomy, deep brain electrical stimulation of GPi and STN

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18
Q

Alzheimer’s

A

Clinical Presentation: Slow-onset memory loss, progressive disorientation, loss of learned motor skills and language, behavior and personality changes
MOA: e4 allele of APOE increases risk of sporadic form; beta amyloid plaques from APP processing aggregate; phosphorylated tau aggregate.
Histo: Cerebral atrophy with gyri narrowing; neuritic plaques of A-beta amyloid derived form amyloid precursor protein; neurofibrillary tau tangles; inflammation, Hirano bodies; hydrocephalus
Tx: Donepezil (Aricept) Memantine (Namenda)
*e2 allele of APOE decreases risk of sporadic form

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19
Q

Lewy Body Dementia

A

Clinical Presentation: Dementia, fluctuations in cognition and arousal, and visual hallucinations; Parkinsonism; REM sleep behavior disorder
Histo: Intracellular Lewy bodies in cortex; aggregates of alpha-synucleins
*ApoE4 allele is a risk factor

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20
Q

Frontotemporal Lobar Degeneration

A

Clinical Presentation: Progressive language deterioration, personality changes
MOA: Atrophy of frontal and temporal lobes
Histo: Many contain tau deposits

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21
Q

Pick Disease (Frontotemporal lobe Dementia)

A

Clinical Presentation: Inappropriate social behavior, lack of empathy, distractibility, loss of insight, repetitive or compulsive behavior, decreased motivation, language disturbance
MOA: Degeneration of frontal and temporal lobe; spares parietal and occipital lobe

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22
Q

Dementia

A

Clinical Presentation: Cognitive deficits, acquired after age 18, persistent and multiple areas affected
MOA: Four most prevalent causes: Alzheimer’s, Parkinson’s, Vascular Dementia, Diffuse Lewy body dementia

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23
Q

Concussion

A

Clinical Presentation: Confusion, headache, balance problems, dizziness, sluggishness, groggy, foggy, amnesia, difficulty paying attention, nausea, vomiting, double/blurry vision, bothered by light or noise
MOA: Strike to head causes rotation of partially tethered brain putting shearing stress on the brain; get transient stretching of axons WITHOUT transection

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24
Q

Diffuse Axonal Injury

A

Clinical Presentation: Slow recovery from concussion symptoms; permanent disability
MOA: Torque from strike to the head causes tearing of the axons; often affects midbrain/diencephalon, corona radiata

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25
Q

Epidural Hematoma

A

Clinical Presentation: Cranial nerve III palsy; 80% are in temporal area; rare in infants and elderly
MOA: Collection of blood between dura and the skull; classically due to fracture of temporal bone with rupture of middle meningeal artery
*lens shaped (biconvex) lesion of CT; not crossing suture lines
*herniation of a lethal complication

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26
Q

Subdural Hematoma

A

Clinical Presentation: progressive neurologic signs
MOA: Blood pooling underneath dura and covers the surface of the brain; due to tearing of bridging veins that lie underneath dura and arachnoid usually b/c of trauma
*crescent-shaped lesion of CT that crosses suture lines
*most are lethal: 30-90% mortality
*herniation is a lethal complication

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27
Q

Subarachnoid Hemorrhage

A

Clinical Presentation: Produces blood in CSF; causes severe headache, stiff neck, loss of consciousness
MOA: typically due to rupture of an aneurysm as arteries pass within subarachnoid space
*acute blood lining cortex in subarachnoid space
*one of the only causes of blood pooling at the bottom/base of the brain

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28
Q

Chronic Subdural Hemorrhage

A

Clinical Presentation: Headache, progressive alteration in mental status, focal neuro signs; common in elderly
MOA: Caused by trauma; common in elderly and the brain shrinks causing stretching/stress of bridging veins
*hyper of isodense area on radiology

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29
Q

Brain Herniation

A

Clinical Presentation:
Central herniation - midsize, bilateral non-reactive pupils
Lateral herniation - unilateral dilated non-reactive pupils
MOA: Edematous brain or hematoma causes compression of brain structures (diencephalon, midbrain, pons, medulla)

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30
Q

Athetosis

A

Clinical Presentation: Slow, writhing movements, especially in fingers
MOA: Lesion to basal ganglia

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31
Q

Chorea

A

Clinical Presentation: Sudden, jerky, purposeless movements
MOA: Lesion to basal ganglia
*dopamine blockers, anticholinergics

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32
Q

Dystonia

A

Clinical Presentation: Sustained, abnormal involuntary movements
MOA: Blapharospasm, torticollis, writer’s cramp

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33
Q

Essential Tremor

A

Clinical Presentation: High frequency tremor with sustained posture (i.e. outstretched arms)
Tx: non-selective beta blockers; pts often self medicate with alcohol
*worse when anxious or with movement; often familial

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34
Q

Hemiballismus

A

Clinical Presentation: sudden, wild flailing of one arm; may also have flailing of ipsilateral leg
MOA: lesion to contralateral subthalamic nucleus

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35
Q

Intention Tremor

A

Clinical Presentation: Slow, zig zag motion when pointing/extending towards a target
MOA: Cerebellar dynsfunction

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36
Q

Akinetic Rigid Syndrome (Parkinsonism)

A

Clinical Presentation: Bradykinesia/akinesia, rigidity, postural instability

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37
Q

Myoclonus

A

Clinical Presentation: sudden, brief, uncontrolled muscle contraction

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38
Q

Resting Tremor

A

Clinical Presentation: Uncontrolled movement of distal appendages; tremor alleviated by intentional movement
MOA: Parkinson’s

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39
Q

Rigidity

A

Clinical Presentation: Sustained muscle contraction at rest (in the absence of any voluntary movement)

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40
Q

Spasticity

A

Clinical Presentation: Little or no contraction at rest

MOA: Late phase of spinal cord transection; corticospinal lesion

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41
Q

Tardive Dyskinesia

A

Clinical Presentation: Abnormal involuntary movements

MOA: After the use of dopamine blocking agents

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42
Q

Multiple Sclerosis

A

Clinical Presentation: Neuro deficits with periods of remission; blurred vision in one eye, vertigo, scanning speech, hemiparesis; internuclear ophthalmoplegia; lower extremity loss of sensation or weakness
MOA: Autoimmune destruction of CNS myelin and oligodendrocytes; associated with HLA-DR15
MRI: periventricular plaques (areas of white matter de-myelination); CSF: increased lymphocytes, increased Ig and myelin basic protein; Histo: macrophages, thin myelin
Tx: high dose steroids for acute attacks; interferon beta long term slows progression of disease

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43
Q

Acute MS

A

Clinical Presentation: Affects kids to young adults; mimics a high grade neoplasm

  • relatively unresponsive to steroids
  • death sometimes in days to weeks
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44
Q

Adrenoleukodystrophy

A

Clinical Presentation: Often occurs in young boys; progressive intellectual and behavioral problems
MOA: Impaired addition of coenzyme A to long chain fatty acids (X-linked mutation of ABCD1 transporter gene); accumulation of fatty acids damages adrenal glands and white matter of brain
Histo: perivascular CD8+ T-lymphocytes; macrophages, adrenal cortical cells, and Leydig cells with trilaminar lipid inclusions; glial scar

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45
Q

Acute Disseminated Encephalomyelitis (ADEM)

A

Clinical Presentation: Rapidly progressive multifocal neuro symptoms; altered mental status; affects children and young adults
MOA: Multifocal periventricular inflammation and demyelination after infection of vaccine; may be auto-immune reaction
Histo: small perivascular foci of myelin loss
Tx: steroids, plasmapheresis, IVIG

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46
Q

Progressive Multifocal Leukoencephalopathy

A

Clinical Presentation: Rapidly progressive neurologic signs (visual loss, weakness, dementia) leading to death
MOA: JC virus infection and destruction of oligodendrocytes (white matter); immune suppression reactivates the latent virus
Histo: Oligodendrocytes with viral inclusions
*typically short course (6-12 months) that leads to death

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47
Q

Central Pontine Myelinolysis

A

Clinical Presentation: Rapid quadriplegia; only eyes move; dysphagia, diplopia, loss of consciousness
MOA: Metabolic demyelination of pons due to rapid osmotic changes (rapid IV correction of hyponatremia, liver transplant, alcoholism)
*occurs in severely malnourished patients (i.e. alcoholics, liver disease)

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48
Q

Neuromyelitis Optics (NMO)

A

Clinical Presentation: Optic neuritis and myelitis; can involve outside the CNS as well
MOA: Autoimmune attack of aquaporin 4 (astrocytic water channel)
MRI: contiguous spinal cord lesion for 3+ segments
Histo: Creutzfeldt cells (macrophages with mitotic figures), thin myelin

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49
Q

Acute Hemorrhagic Encephalomyelitis

A

Clinical Presentation: Abrupt onset of fever, neck stiffness, seizures, cerebral swelling
MOA: Children and young adults after upper respiratory tract infection, vaccine, or drug reaction
*possibly fulminant form of ADEM

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50
Q

Alexander Disease

A

Clinical Presentation:
Young children - seizures, spasticity, megaencephaly, developmental delay
Older patients: brain stem symptoms
MOA: AD inheritance; mutation in GFAP gene
Histo: White matter demyelination, Rosenthal fibers to the max, disorder of astrocytes

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51
Q

Conductive Hearing Loss

A

Impaired conduction of sound through external and middle ear; impacted cerumen, otitis media, otosclerosis
Dx:
Webber test - sound is louder in ear with conductive loss
Rinne test - won’t hear when fork is held outside of ear

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52
Q

Sensorineural Hearing Loss

A

Pathology of the inner ear (cochlea, sensory) or CN VIII; Loss of hair cells, perinatal infection, high intensity sounds, ototoxic drugs
Dx:
Webber test - sound quieter in affected ear

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53
Q

Presbycusis

A

Age related; due to the cumulative effect of loud sounds on the ear
Histo: affects higher frequency hair cells first

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54
Q

Meniere’s Disease

A

Clinical Presentation: Fluctuating hearing loss, rotational vertigo, tinnitus, aural fullness
Tx: low salt diet and diuretics

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55
Q

Tinnitus

A

Clinical Presentation: Perception of phantom sound that occurs in the absence of actual sound
MOA: Often seems to be of CNS origin; often accompanies cochlear hair cell loss

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56
Q

Hollywood Amnesia

A

Clinical Presentation: Severe long term memory deficit; preserved short term memory
MOA: Is due to psychogenic issue; NOT caused by a neurogenic problem

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57
Q

Isolate Amnestic Syndrome

A

Clinical Presentation: Short term memory loss
MOA: Often idiopathic; can be due to thalamic damage, basilar occlusion, thiamine deficiency, anoxia, or trauma
*usually goes away on its own fairly quickly

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58
Q

Korsakoff’s Psychosis

A

Clinical Presentation: Little to no acquisition of new information; impaired retrieval of old memories, confabulation

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59
Q

Anophthalmia/Microphthalmia

A

Clinical Presentation: Absence of an eye or presence of a small eye
MOA: SOX2 and PAX6 gene dysfunction

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60
Q

Coloboma

A

Clinical Presentation: Missing part of the iris

MOA: Failure of closure of the choroidal fissure; PAX2 mutations in 50%

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61
Q

Congenital Cataracts

A

Clinical Presentation: Clouding of the lens

MOA: Due to incomplete differentiation of the lens during development

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62
Q

Treacher Collins Syndrome (TCS)

A

Clinical Presentation: Maral hypoplasia (underdevelopment of zygomatic bones): under developed mandible malformed or missing ears, downslanting palpebral fissures
MOA: AD inheritance; due to not enough neural crest cells proliferating and migrating to branchial arches.

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63
Q

Pierre Robin Sequence (PRS)

A

Clinical Presentation: Micrognathia of mandible, cleft palate, glossoptosis (posterior displaced tongue)
MOA: Defect in neural crest cell affecting mandible development; environmental and genetic factos
Tx: Palatoplasty mandibular distraction; avoid respiratory distress

64
Q

DiGeorge Anomaly

A

Clinical Presentation: CATCH-22. Cardiac outflow tract abnormalities, Abnormal facies, Thymic aplasia, Cleft palate, Hypoparathyroidism, Chromosome 22
MOA: Deletion of long arm of chromosome 22 (22q11) causing errors in the development of the branchial arches

65
Q

Hemifacial Microsomia

A

Clinical Presentation: Malformed auricle (microtia/anotia);ossicluar malformation, facial muscle asymmetry, hyoid malformation
MOA: Anomaly of development of the second branchial arch

66
Q

First Pouch Anomaly

A

Clinical Presentation: Eustachian tube dysfunction, recurrent ear infection, absent tympanic cavity, absent mastoid cavity
MOA: Anomaly of development of the first branchial pouch

67
Q

Thyroglossal Duct Cyts

A

Clinical Presentation: Asymptomatic midline neck mass that may move/elevate with protrusion of the tongue
MOA: Anomaly of development of the 3rd/4th branchial pouch; failure of complete obliteration of the thyroglossal duct
Tx: Remove surgically
*found in 7% of the population

68
Q

Lingual Thyroid

A

Clinical Presentation: Reddish mass at the base of the tongue
MOA: Complete failure of thyroid descent (anomaly of 3rd/4th branchial pouch development)
Tx: Remove thyroid tissue surgically and use thyroid replacement hormone

69
Q

Type 1 First Cleft Anomaly

A

Clinical Presentation: Sinus or cyst anterior to ear canal, ends blindly at ear canal, enters ear canal, or middle ear space; lateral to CN VII
MOA: Anomaly of first branchial cleft development

70
Q

Type 2 First Cleft Anomaly

A

Clinical Presentation: Sinus or cyst at angle of mandible, ends in ear canal, lateral or medial to CN VII
MOA: Anomaly of first branchial cleft development
*more common

71
Q

Second Cleft Anomaly

A

Clinical Presentation: Painless, fluctuant cyst, sinus, or fistula in anterior triangle
MOA: Anomaly in 2nd branchial cleft development

72
Q

Third/Fourth Cleft Anomaly

A

Clinical Presentation: Sinus/fistula in lower third of anterior neck that ends in piriform sinus; associated with thyroid gland
MOA: Anomaly in 3rd/4th branchial cleft development
Tx: Hemithyroidectomy, direct laryngoscopy, endoscopic cauterization

73
Q

Broca’s Aphasia

A

Clinical Presentation: Non-fluent speech, comprehension is normal, difficulty repeating words
MOA: Damage to Broca’s area (in anterior multi-modal association area), such as due to an MCA stroke/hemorrhage

74
Q

Wernicke’s Aphasia

A

Clinical Presentation: Speech is fluent but nonsensical, distorted comprehension, cannot repeat words
MOA: Damage to Wernicke’s area (in posterior multi-modal association area)

75
Q

Conduction Aphasia

A

Clinical Presentation: Fluent speech, normal comprehension, cannot repeat words
MOA: Damage to the tract connecting Broca’s and Wernicke’s area

76
Q

Trans-cortical Sensory Aphasia

A

Clinical Presentation: Fluent speech, poor comprehension, can repeat words
MOA: Disconnection of Wernicke’s area from the rest of the multi-modal association area

77
Q

Trans-cortical Motor Aphasia

A

Clinical Presentation: Non-fluent speech, normal comprehension, can repeat words
MOA: Disconnection of Broca’s area from the rest of the multi-modal association area

78
Q

Paranoid Personality Disorder

A

Group A

Pattern of irrational suspicion and mistrust of others; interpreting motivations as malevolent

79
Q

Schizoid Personality Disorder

A

Group A

Lack of interest and detachment from social relationships; restricted emotional expression

80
Q

Schizotypal Personality Disorder

A

Group A
Extreme discomfort interacting socially, distorted cognitions and perceptions, behavioral eccentricities, magical thinking
Gross: see compromise of temporal lobe and basal striatothalamic structures

81
Q

Antisocial Personality Disorder

A

Group B
Pervasive pattern of disregard for violation of the rights of others, lack of empathy
MOA: must first have history of conduct disorder in childhood
*childhood physical, parental marital abuse, poverty, and foster care are associated

82
Q

Borderline Personality Disorder

A

Group B
Instability in relationships, self-image, identity, behavior, and affect; often leads to self harm and impulsivity
*40-70% have had childhood sexual abuse; see lower volume of hippocampus, LPFC, and cingulate

83
Q

Histrionic Personality Disorder

A

Group B

Attention seeking behavior and excessive emotions; seduction/manipulation of others

84
Q

Narcissistic Personality Disorder

A

Group B

Pattern of grandiosity, need for admiration, lack of empathy

85
Q

Avoidant Personality Disorder

A

Group C

Feelings of social inhibition and inadequacy, extreme sensitivity to negative evaluation, strong social anxiety

86
Q

Dependent Personality Disorder

A

Group C

Psychological need to be care for by other people

87
Q

Obsessive Compulsive Personality Disorder

A

Group C

Rigid conformity to rules, perfectionism, and control

88
Q

Superior Division of MCA Stroke

A

Clinical Presentation: Contralateral hemiparesis of face, hand, and arm; contralateral hemisensory deficit of face, hand, and arm; ipsilateral deviation of head/eyes
MOA: Affects the precentral and postcentral gyrus; affects from the waist up

89
Q

Inferior Division of MCA Stroke

A

Clinical Presentation:
Dominant Hemisphere - Wernicke’s aphasia
Non-Dominant Hemisphere - visual field neglect, agitated and confused state; superior quadrantanopsia
MOA: Loss of blood supply to lateral surface of temporal lobe below the lateral sulcus

90
Q

Anterior Cerebral Artery Stroke

A

Clinical Presentation: Paraplegia of lower extremities; frontal lobe syndrome (abuilia - loss of will power, inability to make decisions, personality change); urinary incontinence
MOA: Motor and sensory cortices lesion affecting lower limb

91
Q

Lenticulostriate Artery Stroke

A

Clinical Presentation: Contralateral hemiparesis and sensory deficit; contralateral ataxia; contralateral lower face hemiparesis
MOA: Loss of blood to basal ganglia structures; part of head and body of caudate, globus pallidus, putamen, and internal capsule

92
Q

Anterior Spinal Artery Stroke

A

Clinical Presentation: Medial medullary syndrome
MOA: stroke causes damage to the lateral corticospinal tract, medial lemniscus, and hypoglossal nerve/nucleus in medial medulla

93
Q

Posterior Inferior Cerebellar Artery Stroke

A

Clinical Presentation: Lateral medullary syndrome (Wallenberg’s Syndrome)
MOA: PICA stroke damaging AL fibers, spinal trigeminal tract and nucleus, nucleus ambiguous, descending hypothalamic fibers, vestibular nuclei, inferior cerebellar peduncle, and spinocerebellar fibers in lateral medulla

94
Q

Paramedian Branch of the Basilar Artery Stroke

A

Clinical Presentation: Medial pontine syndrome

MOA: Leads to damage to ML, corticospinal fibers, abducens nerve/nucleus found in medial pons

95
Q

Long Circumferential Branch of Basilar Artery Stroke

A

Clinical Presentation: Lateral pontine syndrome
MOA: Damage to AL fibers, spinal trigeminal tract and nucleus, descending hypothalamic fibers, middle and superior cerebellar peduncles, vestibular and cochlear nerve/nucleus, facial motor nucleus, trigeminal motor/sensory nucleus

96
Q

Paramedian Branch of Basilar Bifurcation Stroke

A

Clinical Presentation: Medial midbrain syndrome

MOA: Damage to ML, corticospinal fibers, oculomotor nerve, and corticobulbar fibers

97
Q

Posterior Cerebral Artery Stroke

A

Clinical Presentation: Contralateral hemianopia with macular sparing
MOA: Occipital cortex or visual cortex lesion

98
Q

Ophthalmic Artery

A

Painless, ipsilateral blindness (often transient)

99
Q

Internal Carotid Artery

A

Altered conscious level, contralateral homonymous hemianopia, hemiplegia, hemisensory disturbance; gaze towards side of lesion; ipsilateral Horner’s Syndrome

100
Q

Acute Alcoholic Gastritis

A

Clinical Presentation: Anorexia, epigastric pain, vomiting

MOA: Alcoholism

101
Q

Acute Alcoholic Pancreatitis

A

Constant epigastric pain, pain worse after eating, low grade fever, epigastric tenderness

102
Q

Alcoholic Fatty Liver

A

Clinical Presentation: Tender, enlarged liver, GGTP, AST, and ALT elevated
*reversible in several weeks with abstinence

103
Q

Alcoholic Hepatitis

A

Jaundice, low grade fever, enlarged, tender liver; persistently elevated AST, ALT, and alkaline phosphate

104
Q

Alcoholic Cirrhosis

A

Clinical Presentation: Jaundice, elevated AST, ALT, billirubin; ascites, peripheral edema, nodular liver
MOA: Scarring of the liver due to chronic alcohol use

105
Q

Alcoholic Polyneuropathy

A

Clinical Presentation: Lower, distal extremities affected; sensory and motor deficits; dysesthesia (“burning feet”)
MOA: May be due to vitamin B complex deficiency (decreased intake and decreased absorption in small intestines)
Tx: Slow improvement (months to years) with abstinence and vitamins

106
Q

Alcoholic Optic Neuropathy

A

Clinical Presentation: Bilateral central scotoma and blurred vision
MOA: May be due to vitamin B complex deficiency (decreased intake and decreased absorption in small intestines)
Tx: Reversible with cessation of alcohol and treatment with vitamin B complex

107
Q

Wernicke’s Encephalopathy

A

Clinical Presentation: CN VI paralysis/palsy; truncal ataxia, confusion
MOA: Thiamine deficiency which can cause cerebellar degeneration

108
Q

Karsakoff’s Syndrome

A

Clinical Presentation: Inability to retain new information
Tx: usually irreversible
*often occurs with Wernicke’s

109
Q

Marchiafava-Bignami Syndrome

A

Clinical Presentation: Coma, seizures, quadriparesis
MOA: Demyelination of anterior and posterior corpus callosum
*very rare
*associated with red wine

110
Q

Migraine

A

Clinical Presentation: Severe pain; unilateral, throbbing quality, nausea, photophobia and phonophobia
MOA: Usually idiopathic; can be neurogenic, vascular or trigeminal
Tx: Analgesics, caffeines, sedatives, anti-emetics, ergotamine, triptans; prophylactic therapy

111
Q

Cluster Headache

A

Severe, uni-lateral peri-orbital 15-180 in untreated headache; associated with conjunctival injection, lacrimation, rhinorrhea, miosis, ptosis, and eyelid edema

112
Q

Tension Headache

A

Mild to moderate pain

Tx: TCAs, SSRIs, SNRIs, analgesics, stress management, exercise

113
Q

Syndrome of Neglect

A

Clinical Presentation: Inability to respond to stimuli on the contralateral side of the body or the contralateral visual field
MOA: Parietal cortex lesion

114
Q

Apraxia

A

Clinical Presentation: Difficulty manipulating objects with the contralateral hand
MOA: Parietal cortex lesion

115
Q

Astereognosis

A

Clinical Presentation: Failure to recognize objects placed in contralateral hand
MOA: Parietal cortex lesion

116
Q

Myasthenia Gravis

A

Clinical Presentation: Fluctuating weakness with abnormal fatiguability that improves with rest; diplopia and ptosis, dysarthria, dysphagia, dyspnea
MOA: Antibody mediated attach on nicotinic acetylcholine receptors preventing Ach from binding and exciting muscle; inhibits NMJ transmission
Tests: Edroponium test, AchR antibody test (most specific), single fiber EMG (most sensitive)
Tx: Cholinesterase inhibitors, immunosuppression, plasmapheresis, IVIG, thymectomy

117
Q

Vestibular Nerve Lesions

A

Clinical Presentation: Subject tends to fall towards the side of the lesion; nystagmus to the contralateral side
MOA: Sets up an imbalance in favor of the opposite side

118
Q

Adiadochokinesis (dysdiadochokinesis)

A

Clinical Presentation: Inability to make rapid, alternating movements
MOA: Lesion to the cerebrocerebellum

119
Q

Acute Cerebellar Ataxia

A

Clinical Presentation: Inability to walk (severe ataxia), headache
MOA: Can develop in children after an illness, often a viral illness
*considered benign; symptoms often diminish within several weeks

120
Q

Pseudo-tumor Cerebri

A

Clinical Presentation: Headache developing over weeks or months; episodic blurred or double vision, papilledema
MOA: Increased flow resistance in arachnoid villi or increased dural sinus pressure; poor absorption of CSF in arachnoid granulations
*normal head imaging

121
Q

Giant Cell Arteritis (Temporal Arteritis)

A

Clinical Presentation: New onset of headaches, temporal artery tenderness, ESR elevated
Histo: Necrotizing arteritis
*can cause blindness

122
Q

Intraparenchymal Hemorrhage

A

Clinical Presentation: Most often at putamen, thalamus, pons, and cerebellum
MOA: Most often caused by HTN; also by accelerated atherosclerosis, hyaline arteriosclerosis, and Charcot-Bouchard aneurysms

123
Q

Subfalcine Herniation

A

Central herniation; anterior cerebral artery compression

124
Q

Transtentorial (Uncal) Herniation

A

CN III compression, PCA compression

125
Q

Schizophrenia

A

Clinical Presentation: Two or more of the following for at least 6 months: delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior, negative symptoms
Histo: Enlarged lateral and 3rd ventricle, reduced hippocampus, amygdala, and parahippocampal gyrus, hypoactive frontal lobe, thalamic disorder
Tx: atypical anti-psychotics

126
Q

Schizophreniform Disorder

A

Same symptoms as schizophrenia but duration is greater than one month and less than 6 months

127
Q

Schizoaffective Disorder

A

Major depressive, manic, or mixed episode occurring simultaneously with characteristic criterion A symptoms of schizophrenia

128
Q

Delusional Disorder

A

Non-bizarre delusion of at least one month; without hallucinations, disorganized speech, catatonic behavior, negative symptoms, or bizarre behavior

129
Q

Brief Psychotic Disorder

A

Delusions, hallucinations, or disorganized speech/behavior for less than a month
Tx: return to full pre-morbid functioning after this brief period

130
Q

Metabolic Coma

A

Clinical Presentation: Small and reactive pupils, absent fast ocular movements, localized motor response
MOA: Toxic metabolic process causing cortical dysfunction

131
Q

Diencephalic Coma

A

Clinical Presentation: Small, reactive pupils, intact slow ocular movements, decorticate motor response
MOA: reticular activating system dysfunction or cortical dysfunction

132
Q

Supratentorial Coma

A

Clinical Presentation:
Early - small reactive pupils, intact slow ocular movements, decorticate motor response
Late - midrange unreactive pupils, abnormal slow ocular movements, decerberate motor response
MOA: Reticular activating system dysfunction or cortical dysfunction

133
Q

Subtentorial Coma

A

Clinical Presentation: Mid-range unreactive pupils, abnormal slow ocular movements, decerberate motor response
MOA: Reticular activating system dysfunction or cortical dysfunction

134
Q

Psychogenic Coma

A

Clinical Presentation: Midrange reactive pupils, intact slow and fast ocular movements, localized motor response

135
Q

Creutzfeldt-Jakob Disease

A

Clinical Presentation: Rapidly progressive dementia with ataxia and startle myoclonus, visual decline, pyramidal dysfunction, akinetic mutism
MOA: Protease resistant prion protein converted to beta Tests: Periodic sharp waves seen on EEG; CSF elevated 14-3-3 protein; MRI increased signal in deep nuclei
Histo: Neuronal loss, gliosis, spongiform change, florid plaques
Tx: no therapies. Results in death

136
Q

Meningitis

A

Clinical Presentation: Headache, nuchal rigidity, fever; photophobia, vomiting, altered mental status, nausea
MOA: Inflammation of leptomeninges (pia and arachnoid layers) most commonly due to group B strep, E. coli, Listeria monocytogenes, N. meningitidis, Strep pneumonia, H. Influenza, Coxsackievirus, Fungi
CSF: Cloudy, neutrophils, increased pressure, increased protein content, decreased glucose
Dx: made by LP
*complications usually seen with bacterial meningitis

137
Q

Brain abscess

A

MOA: Can be caused by staph or strep from endocarditis, congenital heart disease, lung infection, or local sinus infection
Histo: Ring enhancing lesion with white matter expansion, gliosis of white matter
*can look like glioblastoma

138
Q

Toxoplasmosis

A

MOA: T. Gondii protozoan; transferred from cats and their poop
Tests: Necrotic abscesses, free organisms, organisms in cysts; ring enhancing lesion on imaging
*AIDS, organ transplant, malignancy, and those with connective tissue disease are more at risk

139
Q

Cryptococcus Neoformans

A

Clinical Presentation: Subacute or chronic meningitis; hydrocephalus
MOA: Yeast invades the parenchyma, thickening leptomeninges and hydrocephalus
Histo: Mucoid encapsulated yeasts with India ink or PAS stain
Tx: Fluconazole
*85% of sufferers have debilitating illness

140
Q

Herpes Simplex Encephalitis

A

Clinical Presentation: Seen in teens and young adults in temporal and inferior frontal lobes
MOA: Usually caused by HSV-1
Histo: chronic inflammatory cells present
Dx: via CSF PCR

141
Q

Poliomyelitis

A

Clinical Presentation: Flaccid paralysis with muscle atrophy, fasciculations, weakness with decreased muscle tone, impaired reflexes, negative Babinski sign
MOA: Damage to anterior motor horn due to poliovirus infection (an enterovirus)
Histo: Inflammation, neuronophagia of anterior horn cells, no inclusion bodies

142
Q

HIV Encephalitis

A

Clinical Presentation: Diffuse encephalopathy in subset of late stage AIDS
Histo: Microglial nodules, muti-nucleated giant cells

143
Q

Subacute Sclerosing Panencephalitis

A

Clinical Presentation: Cognitive decline, spasticity of limbs, seizures
MOA: Persistent infection by altered measles virus; occurs years after infection
Histo: Gliosis, sclerosis, myelin degeneration, viral inclusions, chronic encephalitis, neurofibrillary tangles

144
Q

Bipolar I

A

Clinical Presentation: Period of abnormally and persistently elevated, expansive or irritable mood lasting one week and 3 or more of the following - inflated self esteem/grandiosity, decreased need for sleep, more talkative, flights of ideas, distractibility, increased goal directed activity
MOA: Glutamate and NE elevation with HPA activation during mania; NE deficiency in depression
Tx: Anticonvulsants, mood stabilizers, lithium, valproic acid, carbamazepine, lamotrigine

145
Q

Bipolar II

A

Clinical Presentation: Period of abnormally and persistently elevated, expansive or irritable mood lasting 4 days and 3 or more of the following - inflated self esteem/grandiosity, decreased need for sleep, more talkative, flights of ideas, distractibility, increased goal directed activity
MOA: Glutamate and NE elevation with HPA activation during mania; NE deficiency in depression
Tx: Anticonvulsants, mood stabilizers, lithium, valproic acid, carbamazepine, lamotrigine

146
Q

Cyclothymic Disorder

A

Clinical Presentation: 2 years of numerous hypomanic episodes and depressive episodes; not without symptoms for more than 2 months at a time
Tx: Anticonvulsants, mood stabilizers, lithium, valproic acid, carbamazepine, lamotrigine

147
Q

Major Depressive Disorder

A 
5 or more of the following for 2 weeks or more: 
- sad/irritable mood
- loss of interest 
- change in appetite or body weight
- difficulty sleeping or oversleeping
- loss of energy
- worthlessness
- difficulty concentrating
Tx: Tricyclics, MAOIs, SSRIs, SNRIs
148
Q

Persistent Depressive Disorder

A

2 year duration of depression, more chronic but less severe; poor appetite or oversleeping, insomnia, hypersomnia, low energy or fatigue, low self-esteem, hopelessness
Tx: Tricyclics, MAOIs, SSRIs, SNRIs

149
Q

Rabies

A

Clinical Presentation: Acute neurological symptoms; brain edema, inflammation
MOA: Virus transported to CNS via intra-axonal transport
Histo: Negri bodies (intra-cytoplasmic inclusions) in Purkinje cells and hippocampus
*fatal in non-immunized hosts

150
Q

Thalamic Pain Syndrome

A

Clinical Presentation: Initial sensory loss followed by excruciating, intractable pain
MOA: Occlusion of the thalamogeniculate artery which supplies latero-posterior half of the thalamus

151
Q

Prosopagnosia

A

Inability to recognize faces, still have measurable emotional response to familiar faces

152
Q

Capgrass Syndrome

A

Consciously able to recognize faces, but no unconscious emotional response to familiar faces

153
Q

Cerebral Amyloid Angiopathy

A

Collection of amyloid protein leads to alteration of vessel wall structure
Histo: Concentric rings of tissue; stain positive with Congo red stain

154
Q

Arteriovenous Malformation

A

Vascular malformation
Histo: Tangle of arteries and veins. Have brain tissue in between the vessels
*not resectable

155
Q

Cavernous Angioma

A

Vascular malformation
Histo: Back to back hyalinized vessels. No brain tissue in between. See hemosiderin deposits.
*resectable

156
Q

Capillary Telangiectasia

A

Dilated thin walled vessels separated by normal brain

157
Q

Cholesteatoma

A

Clinical Presentation: Can present with hearing loss or repeated middle ear infections
MOA: Abnormal skin growth in the middle ear behind the eardrum from repeated infections and/or a tear or pulling inward of the eardrum
Tx: Antibiotics and/or surgery

Brain & Behavior Extras (5 decks)

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