Diseases Flashcards

Question

Epidural hemmorhage

Answer 1

Results from tearing of MMA causing bleeding that dissects the dura from the inner table of skull Associated with skull fracture often of the temporal bone-pterion (facture at frontal, parietal, temporal and sphenoid-bone is thin and MMA courses within the skull at this point) MMA is branch of maxillary artery (of external carotid) enters skull via foramen spinosum Rapidly space occupying lesion death occurs 2-12 hours after injury Causes uncal herniation/ transtentorial herniation and/or downward displacement of brainstem can cause CN III palsy Clinical: Initial unconsciousness followed by lucid interval (seconds to hours) progression to coma Symptoms: focal signs and indications of increases intracranial pressure, less alertness, contralateral hemiparesis and ipsilateral pupillary dilation Imaging: biconvex high density, sharply defined, rarely crosses Sutural margins, may cross midline Between dura and bone

Answer 2

Accompanied by cerebral contusion-worst headache of my life Bloody or yellow CSF may be detected 2-3 days later (xanthochromic) Bleeding raised from small vessels Bruising associated with fracture of the skull Hydrocephalus may result if subarachnoid bleeding or fibrosis obstructs CSF flow Associated with Marfan, Ehlers Danlos, ADPKD, coarctation of the aorta or an AVM of posterior and anterior communicating arteries Risks: vasospasm due to blood breakdown-new onset ischemia, confusion and focal signs-diagnose with transcranial doppler and treat with nimodipine Rebleeding-re development of severe headache, nausea, vomiting, change in consciousness new neurlogical deficits-diagnose with CT Can have blood in basal cisterns also have nuchal rigidity and fever (watch out for meningitis) Between arachnoid and pia

Answer 3

Head injury that may cause unconsciousness, respiratory arrest and loss of reflexes Instantaneous onset Change in momentum of the head is thought to be a critical factor in producing a concussion No parenchymal abnormalities on CT

Answer 4

Area of hemorrhagic necrosis Following a head injury the brain strikes supporting structures and bony projections of skull bruising gyral crests Location: frontal lone orbital surfaces and temporal lobes are most common Produced by rotation of the brain or by linear forces Can be coup or contrecoup lesions Pathology: summit of gyrus is smashed, lesion is wedge shaped with base towards the pia and apex towards white matter, in early stages the hemorrhage remains bright red an surrounding tissue is edematous later becomes brick red and finally orange brown due to deposition of Hemosiderin Dura-arachnoidal adhesions form on the surface and frequently cause post traumatic epilepsy Imaging: high density areas on CT

Answer 5

Acute loss of function of the nerve roots in the Cauda equina usually due to tumor, trauma, herniated lumbar disk (pudendal nerve) Patients present with lower extremity weakness and sensory loss and bowel and bladder incontinence low back pain, saddle anesthesia, loss of anocutaneous reflex, loss of ankle jerk reflex, with plantar flexion weakness Best assessed by MRI Neurosurgical or radiation therapy emergency

Answer 6

painless Opacity of normally clear lens which may develop as a result of aging, metabolic disorders, trauma or hereditary, smoking, alcohol, excessive sunlight, prolonged corticosteroid use, classic galactosemia, galactokinase deficiency, diabetes (sorbitol), trauma, infection

Answer 7

``` Rapid onset of central vision loss most present with ocular pain made worse when moving the eye Affects women and Caucasians more Mean age is 32 Treat with IV corticosteroid Use MRI to determine risk of MS ```

Answer 8

Presents with: nuchal rigidity, photophobia, and headache Purulent exudate in subarachnoid space and along vessels, include neutrophils and bacteria Inflammatory infiltrate in walls of arteries Cellular infiltration of CNs and spinal roots Edema could occur in brain tissue CSF is a sensitive indicator: high pressure (>200), decreases glucose, increased protein, thousands of neutrophils Hyperintensity in sulci and cisterns on FLAIR imaging

Answer 9

Presents with: confusion, headaches, photophobia Viral meningitis Mononuclear exudate CSF indicator: normal or slightly increased pressure, normal glucose, mildly increased proteins, hundreds of mononuclear cells Hyperintensity in sulci and cisterns on FLAIR imaging

Answer 10

Most common epidemic viral encephalitis often in tropical climates Caused by arboviruses generally Animal hosts and mosquito vectors Affects cortex and basal ganglia but can vary

Answer 11

Most common non epidemic form of encephalitis High mortality levels Acyclovir is an effective treatment Symptoms: alterations in mood, memory and behavior due to lesions in the limbic system Lesions involve the inferior and medial regions of the temporal lobes and the orbital gyri of frontal lobes-MRI Necrosis and hemorrhagic regions Peri vascular infiltrates and inclusion bodies are present Diagnosis:PCR of CSF to detect viral DNA Often RBCs are present in CSF due to necrotizing pathology

Answer 12

Affects the nervous system In adults generally causes meningitis Neonates can acquire infection from mom an develop encephalitis

Answer 13

Causes chickenpox in primary infection Establish latent infection in sensory neurons of dorsal root or trigeminal ganglia Reactivation results in painful vesicular skin eruption in dermatome Can cause granulomatous arteritis may cause infarcts Immunosuppressive patients can develop encephalitis or myelitis

Answer 14

Infects the nervous system of fetuses or immunocompromised individuals Opportunistic pathogen in AIDs patients

Answer 15

Infects anterior horn neurons in spinal cord causing motor defects and flaccid paralysis Post polio syndrome can occur after the initial infection up to 20 years later Caused by poliovirus (enterovirus) spread fecal-orally Replicates in oropharynx and small intestine before sperading via bloodstream to the CNS Symptoms: LMN lesion and infection signs Findings: CSF with increased WBCs and slight increase of protein (no CSF glucose change) Virus recovered from stool or throat Live attenuated vaccine produces a strong mucosal secretory IgA response (offers protection at the site of viral entry by inhibiting attachment to intestinal epithelial cells)

Answer 16

Bite of rabid animal Enters CNS by ascent of peripheral nerves Negritos bodies present in pyramidal neurons of hippocampus

Answer 17

Usually caused by pyogenic bacteria:strep and staph Fungi may produce localized areas of intracerebral inflammation termed granulomatous in immunosuppressed Discrete lesions with central liquefactive necrosis, surrounded by inflammatory cells and fibrous tissue, proliferation of small blood vessels, vasogenic edema, fibrolats are recruited, reactive gliosis CSF changes: increased pressure, relatively few cells, mildly elevated white cell count and protein level, normal glucose Clinical: progressive focal deficits, general signs of intracranial pressure Ependymitis and meningitis occur Seizures in approx 50% of cases

Answer 18

All have increases cell count and positive serologic reaction in CSF (VDRL/RPL) 1. Meningovasculitis: infiltration of meninges and vessels by lymphocytes and plasma cells, causes symptoms similar to meningitis or stroke 2. General paresis: atrophy, loss of cortical neurons especially in frontal lobes, gliosis, proliferation of micro glial cells, peri vascular lymphocytes and plasma cells, spirochetes in brain tissue. Symptoms: Mental changes, dementia and headache 3. Tabes dorsalis: inflammatory lesions involving meninges and vessels in subarachnoid space of dorsal nerve roots. Loss of axons and myelin in dorsal roots with wallerian degeneration of dorsal columns Symptoms: lightning pains, sensory deficits, loss of pain sensation and loss of position sense leads to ataxia, argyll Robertson pupils (react to accommodation -constrict to nearby objects but not light) Symptoms: progressive ataxia, arefelxia and loss of bladder function (due to spirochetes damaging midbrain tectum)

Answer 19

50-70% of aids patients develop Cognitive. Motor and behavioral dysfunction including mood disturbances HIV association dementia located in sub cortical areas sparing the cerebral cortex Microscopic changes: diffuse white pallor, peri vascular infiltrates of lymphocytes and macrophages, foci of necrosis, gliosis and/ or demyelination, micro glial nodules macrophages and multinucleated giant cells Virus enters brain via macrophages Neuronal injury occurs via secretion of cytokines and Chemokines Vacuolae myelopathy in the spinal cord in the posterior and lateral columns

Answer 20

Occurs in patients with associated immune suppression or chronic disease Fifth and sixth decades of life Symptoms: Intellectual deterioration and dementia. Also cortical visual symptoms, motor disorders, abnormal movements Death in 2-6 months Normal CSF findings Pathogenesis: Slowly progressive viral encephalitis by JC polymavirus Infections occur during childhood and are largely asymptomatic, persist in kidneys and lymphocytes Restricts replication to glial cells and infects OLIGODENDROCYTES causing demyelination Gross pathology: widespread demyelination Microscopic pathology: inclusion bodies in oligodendroglia nuclei, transformed bizarre astrocytes and gliosis, lesions primarily in sub cortical white matter but also occur in brainstem and cerebellum increased risk associated with natalizumab Polyomavirus: Naked,, DS DNA circular

Answer 21

Progressive encephalitis associated with altered measles virus Onset: 5-20 years occurs in children of young adults . Early age infection with measles Clinical: progressive personality changes, intellectual deterioration, seizures, spasticity of limbs Duration: death in years CSF changes: elevated IgG and antibody tiger against measles is elevated Pathogenesis: persistent nonproductive infection of CNS Microscopic changes: inclusion bodies in oligodendroglia, neurons and astrocytes. Peri vascular cuffing by lymphocytes and plasma cells, paramyxovirus nucleocapsid tubules characteristic of measles in inclusion bodies

Answer 22

Absence of brain of all parts except basal ganglia, brainstem and cerebellum Open calvarium Increased alpha fetoprotein Polyhydramnios (no swallowing center in brain) Associated with maternal diabetes type I Failure of anterior neuro pore to close Occurs with raschischis which is the failure of Vertebral canal to fuse Folate supplementation decreases risk

Answer 23

Meninges and spinal cord protrude through defect in vertebral column Most lumbosacral Accompanying hydrocephalus and Arnold chiari malformation (downward displacement of cerebellum tonsils through foramen magnum causing non communicating hydrocephalus Non lethal-most common

Answer 24

Meninges and brain tissue protrude through a skull defect | Midline

Answer 25

Clusters of neurons in abnormal locations Associated with seizure disorder Can be in cerebellum and dentate nucleus Failure of migration of nerve cells from sub ependymal region to cortex

Answer 26

Cerebral hemispheres fail to divide properly (malformation) Most sporadic but can have autosomal dominant inheritance One mutation involves sonic hedgehog gene- which produces intercellular signaling Moderate=cleft lip/palate, Severe=cyclops Associated with trisomy 13, 18 and consequence of Fetal Alcohol syndrome

Answer 27

Type II: Herniation of cerebellar tonsils and vermis through foramen magnum Defect in neural tube closure Small posterior fossa Misshapen midline cerebellum Elongation of medulla pons and 4th ventricle Kinking medulla (difficulty swallowing, dysphonia, stridor and apnea) Malformation of colliculi Acqueductal stenosis leads to hydrocephalus Associated with meningomyeolocele and hydrocephalus (can lead to mental impairment) Type I:low lying cerebellar tonsils extend below the forament magnum into vertebral canal Asymptomatic in infants adults have headaches and ataxia Associated with syringomyelia

Answer 28

Large posterior fossa Malformation of cerebellum vermis with midline cyst replacing vermis Lateral displacement of cerebellar hemispheres by enlarged 4th ventricle Hydrocephalus in forebrain Lined by ependymal and arachnoid mater Associated with spina bifida

Answer 29

Not a specific disease entity Non progressive motor deficit 90% congenital; 1/3 premature 10% acquired Pathology: hemmorhages and infarctions, may occur in white matter of hemispheres, may result in weakness or movement disorders Causes: prenatal and perinatal infection, trauma, asphyxia, maternal high BP or diabetes, hemorrhages and infarcts Diagnosis: does not hit milestones after birth, difficulty in maintaining body temp, extreme irratiablity, frequent gagging Management: maximize functional abilities of patients Types: Spastic-most common, increased tone, jerky movements, more severe in lower limbs than in upper limbs. Cross over gait Ataxic- incoordination, imbalance, poor muscle tone, unsteady and shaky Athetoid: involuntary movements, difficulty maintaining posture, irregular movements of face, upper body and arms Hyperbilirubinemia is a common cause

Answer 30

Neuronal storage disease Prevalent among Ashkenazic Jews Deficiency if hexosaminidase A Accumulation of GM2 gangliosides Onset: 3-8 months Clinical: seizures, exaggerated startle reflex, macular cherry red spot, motor incoordination, mental deterioration 1-2 years vegetative state is reached and death at 2-3 years Pathology: lysosomal storage vacuoles in neurons, ballooned cell body, primarily in gray matter

Answer 31

AR Neuronal storage disease Deficiency of galactocerebroside B-galactosidase Accumulation of psychosine and galactocerebroside Onset: 3-6 months Clinical: motor deterioration, feeding difficulties, seizures, crying, irritability, optic atrophy Pathology: decreased myelin in CNS and peripheral nerves Globoid cells Loss of white matter

Answer 32

Most common inherited ataxia-Autosomal recessive GAA repeat expansion in an intron-Frataxin gene (Iron binding protein)-unstable triplet repeat associated with IMM-mitochondrial impairment Onset: 2-16 years Lesions in DRG dorsal columns, spino cerebellum tracts 95% clumsiness is first sign Dysarthria follows 55% pes cavus deformity, otherwise, weakness, sensory loss in limbs, cardiac hypertrophy (CHF and arrhythmias cause of death) and skeletal abnormalities (kyphoscoloiosis), loss of deep tendon reflexes Atrophy of spinal cord Loss of axons and myelin in posterior columns, spinocrebellar tracts and corticospinal tracts Degeneration of the cerebellar dentate nucleus Diabetes mellitus can develop

Answer 33

Deficiency of arylsulfatase A Accumulation of sulfatides Onset: late infantile most common Clinical: progressive mental and motor deterioration, peripheral neuropathy Pathology: widespread myelin deficit in white matter

Answer 34

White pupil No red reflex Infantile cataract most common Can be hereditary, trauma, metabolic error Interrupts normal process of visual development Obtain dilated fundus exam for retinoblastoma diagnosis

Answer 35

Uncontrolled arm and leg movements Excessive dopamine stimulation in diseased brain Linked to each dose of levodopa Treatement: reduce levodopa dose, add dopamine agonist, amantidine, deep brain stimulation to pallidum and subthalamic nucleus

Answer 36

Secondary Parkinsonism Wet wobbly and wacky Communicating hydrocephalus-expansion of ventricles disorts the fibers of corona radiata Gait disturbance and incontinence (occur first due to traction of sacral motor fibers-distinguishes from Alzheimers) Short term memory loss and emotional blunting (due to disension of periventricular limbic system) Enlarged ventricles-due to gradual decline in resorptive capacity of arachnoid villi with slow CSF accumulation can be reversed

Answer 37

Progressive neurodegenerative disorder Onset: middle to old age 4 cardinal features: resting tremor, bradykinesia, rigidity, gait instability ASYMMETRICAL (TRAP) Impaired function of nigrostriatal dopamine neurons Non-motor features: mood disorder, dementia and dysautonomia, impaired function on non dopamine neurons Olfactory dysfunction, constipation and sleep disorders occur before motor deficits Pathology: degeneration of pigmented brainstem neurons-substantia nigra, Lewy bodies in neurons (round eosinophilic and filled with a-synuclein, reduced) brain decreased dopamine in striatum Epi: second most common progressive neuro degenerative illness, slightly more common in men Risk factors: age, severe head trauma, family history, exposure to pesticides, well water, rural living, heavy metals, Von economos encephalitis, MPTP and low uric acid Treatment: levodopa/Caribidopa, dopamine agonists, MAO-B inhibitor maybe amantidine and anticholinergics Progression: slowly worse, motor fluctuations, dyskinesia

Answer 38

``` Akinetic rigid syndrome Asymmetric rigidity Apraxia Myoclonus Alien limb Rare, gaze palsy ```

Answer 39

Akinetic rigid syndrome confused with Parkinson's Rapid, Early falls, down gaze paresis, axial rigidity, truncal apraxia, wide eyed unblinking face, executive function loss males more often affected Only 20% respond to levodopa Pathology: accumulation of hyper-phosphorylated tau protein in neurons neuronal degeneration in midbrain and frontal subcortical white matter neurofiibrillary inclusions in neurons and glia

Answer 40

Sustained and/or phasic contraction of muscle causing abnormal posture or repetitive movements Sensory trick to fix problem Co-contraction of agonist-antagonist muscle Idiopathic: Childhood onset

Answer 41

Autosomal recessive hereditary disease confused with Parkinson's (Chromosome 13) Onset: adolescence Deficient copper excretion-copper transporter gene defect High serum/urine copper, low ceruloplasmin Copper deposition in: Liver-hepatic failure Basal ganglia-Akinetic rigid wing beating tremor Dystonia, chorea Psychiatric problems mimics schizophrenia Descemets membrane:Kayser fleischer ring in eye Some extent symptoms are reversible Gross Pathology: atrophy and discoloration of putamen and globus pallidus Microscopic pathology: neuronal loss and gliosis in putamen

Answer 42

Rapid large amplitude, unilateral, proximal flinging movements Sudden onset stroke in contralateral subthalamic nucleus

Answer 43

``` Vocal and motor tics Affects males more before 20 yoa Autosomal dominant with low penetrate Associated with OCD Treatment: alpha-1 adrenergic receptor agonists, dopamine antagonists, Botox injections, or no treatment ```

Answer 44

Causes chorea (bursts of movement) Occurs between 30-50 Lesions in: caudate, putamen, globus pallidus, and cerebral cortex Pathogenesis: deficiency of GABA, ACh, enkephalin and substance P Trinucleotide CAG expansion-autosomal dominant higher repeats more common in paternal lineage and earlier onset (happens during spermatogenesis) Polyglutamine accumulation and inclusions leads to pathological interactions with other proteins increased histone deacetylation silences neurons needed for survival preventing gene transcription of genes coding neutrophic factors More severe symptoms with successive generations Chorea, psychiatric (depression, dementia, psychosis, aggression) and cerebellar features, athetosis (snakelike movements of fingers) Atrophy of caudate nucleus-box-car ventricles-dilation of frontal honrs of lateral ventricles Loss of neurons in caudate, putamen, globus pallidus and cerebral cortex Suicide is common form of death

Answer 45

Cavity in the cervical spinal cord Occurs at cervical levels (C8-T1) Loss of pain and temp symmetrically in the hands and wasting of hand muscles Encroachment of the cystic cavity in the cord on the anterior commisure Upper extremity weakness and hyporeflexia Lower extremity weakness and hypereflexia Kyphoscolioisis Can affect lateral corticospinal tract Associated with chiari type I malformation: cerebellar ectopia

Answer 46

Mostly autosomal dominant slowly progressive incoordination of gait associated with poor coordination of hands, speech and eye movements. Atrophy of the cerebellum. Lesions in spinal cord and peripheral nerves Caused by expansions of CAG repeats which encode polyglutamine regions in proteins

Answer 47

Etiolgies: HITAAAA clinical presentation: smooth progressive from mins to hours Altered level of consciousness High attenuation on CT Putaminal-most common site, contralateral hemiparesis Thalamic->3.3 cm usually fatal, contralateral hemisensory

Answer 48

Etiology: atherosclerosis, stenosis, embolus Third leading cause of death after non cerebral cardiovascular disease and cancer Imaging: vascular distribution looks hypodense on CT, can be associated with hemorrhage Findings on cat may not be present within 24 hrs Earlier detection on diffusion weighted MRI Ct rules out thrombolysis MRI with perfusion assesses for irreversibly injured tissue

Answer 49

Abnormal communicating vessels-congenital Present initially with hemorrhage Combo of CT, MRI, MRA and conventional contrast angiography

Answer 50

Heritable disorder Caused by combination of volatile anesthetics and NMJ blocking agents Can lead to death Symptoms: tachycardia, hypertension, severe muscle rigidity, hyperthermia, hyperkalemia, acid base imbalance Dantrolene treats the increase in free Ca2+ concentration

Answer 51

Abrupt vision loss, headache, jaw pain, Diagnosis: Erythrocyte sedimentation rate elevated Looking for giant cells in temporal artery biopsy Opthalmic emergency Treatment: long term steroids

Answer 52

Due to liver dysfunction elevated serum ammonia levels Ammonia crosses BBB and is neurotoxic Leads promptly to neurological symptoms, coma and them death Major contributor to hepatic encephalopathy

Answer 53

Cavernous hemangiomas in skin,mucosa, organs; bilateral renal cell carcinomas, hemangioblastomas in retina,brain stem, cerebellum, and pheochrmocytoma Autosomal dominant Mutated vhl tumor suppressor gene on chromosome 3 Constitutive expression of HIf Vacuolated cells

Answer 54

Meneinges but not the spinal cord herniate through spinal canal defect Normal AFP Associaed with Valproate which inhibits folate absorption

Answer 55

Complete loss of contralateral sensory Severe proprioception defects leads to unsteady gait and falls Incomplete lesions or partial resolution leads to painful stimuli on affected side

Answer 56

Voluntary movement of extremetities Propensity to fall toward injured side (ipsilateral side)

Answer 57

lesions involving vermis, fastigial nuclei and/or the flocculonodular result in truncal ataxia, nystagmus and head tilting May have wide based gait and deficits in truncal coordination Bilateral motor deficits affecing axial and proximal limb musculature

Answer 58

Paraneoplastic (autoimmune) Associated with lung, breast, ovarian, and uterine cancer Progressive worsening dizziness, lung and truncal ataxia, dysarthia, and visual disturbances Immune response to tumor cross reacts with purkinje neuron Ags leading to degeneration of cerebellum Anti-yo, anti P/Q, anti Hu Abs in serum

Answer 59

Slow writhing movements especially in fingers Lesion in basal ganglia

Answer 60

Sudden brief uncontrolled muscle contraction Jerks, hiccups, Common in renal and liver failure

Answer 61

Cervical=spasmotic torticollis Sustained involuntary muscle contractions sometimes painful Can be suppressed by opposing action May be basal ganglia lesion Ex: writers cramp, sustained eyelid twitch

Answer 62

Action tremor exacerbated by holding posture/limb position ``` Genetic predisposition (AD) Patients often self medicate with alcohol which decreases tremor amplitude ``` Treatment: beta blockers, primiodone

Answer 63

Uncontrolled movement of distal appendages (most noticeably hands) Tremor alleviated by intentional movement Seen in parkinson's disease

Answer 64

Slow, zig zag motion when pointing/extending toward a target Cerebellar dysfunction

Answer 65

Sudden, jerky purposeless movements Lesion in basal ganglia

Answer 66

Failure of bony spiral canal to close but no structural herniation usually at lower vertebral levels Dura still intact associated with dandy walker Associated with tuft of hair or skin dimple at level of bony defect

Answer 67

Neuropores fail to fuse in the fourth week Associated with low folic acid intake Elevated a-fetoprotein in aminiotic fluid and maternal serum increased Acetylcholinesterase in amniotic fluid Anterior: encephalopathy, ancephaly Posterior=spina bifida, menigocele, menigomyelocele, rachischis (failure of vertebral column to fuse)

Answer 68

Motor: nonfluent aphasia with good comprehension and repetition (Brocas cant repeat) Sensory: poor comprehension with fluent speech and repetition Mixed: nonfluent speech, poor comprehension, good repetition

Answer 69

Profound hypotension affects watershed areas-appear as bilateral wedge shaped bands of necrosis over cerebral convexity lateral to interhemispheric fissure Interruption for 10 seconds leads to syncope 4-5 mins leads to permanent damage Gray matter affected first Hippocampus also affected Upper/leg upper arm weakness, defects in higher-order visual processing

Answer 70

Abnormal dilation of artery due to weakening of vessel wall Occurs at bifurcation of circle of willis-Anterior communication and ACA are most common Rupture leads to subarachnoid hemorrhage (worst headache of my life) or hemorrhagic stroke can also cause bitemporal hemianopia with compression of optic chiasm Associated with ADPKD, Ehlers Danlos Syndrome, an Marfan syndrome risk factors: advanced age, hypertension, smoking, increased in blacks Blood can be found in CNS

Answer 71

Associated with chronic hypertension Affects small vessels-basal ganglia and thalamus

Answer 72

Neuropathic pain due to thalamic lesions Initial sensation of numbness and tingling follwed in weeks to months by allodynia (oridinarily painless stimuli cause pain) and dysaethesia (abnormal sense of touch) occurs in 10% of stroke patients

Answer 73

RECURRENT lobar hemorrhages in elderly B-amyloid deposited in arterial wall leading to weakening of wall and predisposition to rupture Recurrent hemorrhagic stroke most common presentation-less severe located in cerebral hemispheres

Answer 74

Complication of premturity Can lead to neurodevelopment impairment infants born before 32 weeks or BW

Answer 75

Poor repetition but fluent speech, intact comprehension (can't repeat phrases no ifs and or buts) Damage to left superior temporal lobe and/or left supramarginal gyrus

Answer 76

Nonfluent aphasia with intact comprehension Broca area-inferior frontal gyrus of frontal lobe Repetition impaired Right hemiparesis MCA impaired

Answer 77

Fluent aphasia with impaired comprehension and repitition Wernicke area-superior temporal gyrus of temporal lobe Words make no sense Right superior quadrant field defect MCA impaired

Answer 78

Nonfluent aphasia with impaired comprehension Both Broca and Wernicke areas affected

Answer 79

Rupture of bridging veins Slow venous bleeding-less presssure hematoma develops over time Seen in elderly, alcoholics, blunt trauma, shaken baby syndrome (brain atrophy, shaking whiplash) Babies will also have bilateral retinal hemorrhages Crescent shaped hemorrhage that crosses suture lins Midline shift Cannot cross falx, tentorium Between dura and arachnoid gradual onset of headache and confusion

Answer 80

Brief reversible episode of focal neruologic dysfunction lasting

Answer 81

Hemisection of spinal cord Ipsilateral UMN signs below the level of the lesion (corticospinal tract damage) Ipsilateral loss of tactile, vibration, proprioception 1-2 levels below the level of lesion (dorsal column damage) Contralateral pain and temperature loss below the level of lesion (spinothalamic tract damage) Ipsilateral loss of all sensation at the level of the lesion Ipsilateral LMN lesion at level of lesion Above T1 may present with Horner Syndrome

Answer 82

Sympathetic dysfunction Ptosis (superior tarsal muscle) Anihidrosis: absence of sweating and increased flushing on affected side of face Miosis: pupil constriction Hypothalamus to lateral horn (1st synapse) lateral horn to superior cervical ganglion (2nd synapse) Then to smooth muscle of eyelid, sweat glands to forehead/face, pupillary dilator muscle Associated with spinal cord lesions above T1-pancoast tumor, brown sequard, late stage syringomyelia

Answer 83

L2=Conus medullaris Caused by disk herniation, tumors and fractures Flaccid paralysis of bladder and rectum, impotence and saddle anesthesia

Answer 84

Mass effect, fistula or thrombosis Ophthalmoplegia (paralysis of extraocular muscles) and decreased corneal and maxillary sensation with normal visual acuity CN VI commonly affected

Answer 85

Obstruction of external sound vibrations Rinne test: Abnormal-Bone greater than air Weber test: Louder sound in affected ear Causes: cerumen impaction, cholesteatoma, otosclerosis, external or middle ear tumors, tympanic membrane rupture, severe otitis media

Answer 86

Inner ear, cochlea or auditory nerve damage Rinne test: normal air greater than bone Weber: louder sound in unaffected ear Causes: Meinere's disease, acoustic neuroma, presbyscusis, ototoxic drugs

Answer 87

Damage to sterocilliated cells in organ of Corti Prolonged exposure to noises greater than 85dB Acoustic reflex dampens effects of prolonged noise because the stapedius and tensor tympani muscles contract lessening ossicles response to sound Loss of high frequency sound first Sudden exposure to loud noises can cause tympanic membrane rupture

Answer 88

CN VII innervates stapedius muscle via stapedius nerve paralysis of stapedius causes the stapes to ossicillate more widely-hyperacusis patients present with increased sensitivity to everyday sounds and will withdrawal socially treatment: retaining therapy using broadband noise (white noise) CN V3 innervates tensor tympani (sphenoid bone to malleus) which contracts tympanic membrane dampening sound

Answer 89

Refractive error that improves with glasses Hyperopia: eye too short for refractive power of cornea and lens light is focused behind the eye Farsightedness: distant objects seen clearly (too short and hyper so he fell FAR behind)

Answer 90

Refractive error corrected with glasses Nearsightedness: can see near objects Eye too long for refractive power of cornea and lens Light focused in front of retina (My you're long! You shouldn't be so NEAR the front

Answer 91

Abnromal curvature of cornea resulting in different refractive power at different axes

Answer 92

Decrease in focusing ability during accommodation due to sclerosis and decreased elasticity

Answer 93

Acute, painless, monocular vision loss Retina cloudy with attenuated vessels and cherry-red spot at fovea (macula supplied by choroid artery of MCA) Vision loss includes entire visual field and is permanent Most common cause: embolism

Answer 94

Optic disc atrophy with characteristic cupping, with increased Intraocular pressure and poregressive visual field loss Chronic glaucoma Gradual increase in fluid in anterior and posterior chambers Canal of schlemm is still open but drainage is slow Associated with increased age, African American race, family history Painless Primary: unclear cause Secondary: Blocked trabecular meshwork from WBCs (Uveitis),, RBCs (vitreous hemorrhage), retinal elements (retinal detachment)

Answer 95

Acute Optic disc atrophy with charaacteristic cupping, increased intraocular pressure and progressive peripheral visual field loss increase pressure in just posterior chamber Primary: enlargement or forward movement of lens against iris obstruction of aqueous flow through pupil-fluid builds up behind iris, pushing peripheral iris against cornea and impeding flow through trabecular meshwork Painful, sudden vision loss, halos around light, rock-hard eye, frontal headache-do not give epihephrine due to mydriasis Secondary: hypoxia from retinal disease (diabetes, or vein occlusion) induces vasoprliferation in iris that contracts angle Precipitated by anti-cholinergic medicatiotns

Answer 96

Separation of nerosensory layer of retina (photorecpetor layer with rods and cones) from outermost pigmented epithelium (normally shields excess light, supports retina) leads to degeneration of photoreceptors and vision loss May be secondary to retinal breaks, diabetic traction, inflammatory effusions Breaks more common in patients with high myopia and are often preceded by posterior vitreous detachment (flashes and floaters) and eventual monocular loss of vision surgical emergency

Answer 97

Degeneration of macula (central area of retina) Macula is densely packed with cones and has increased visual acuity, no blood vessels Projects to single bipolar cell Causes distortion and eventual loss of central vision (scotomas) (visual defect surrounded by an unaffected eye) Dry: (more common) deposition of yellowish fatty tissue beneath Bruch membrane and retinal pigment epithelium with gradual loss in vision (impaired driving and reading) Due to chronic oxidative damage to retinal epithelium and choriocapillaries Prevent progression to "wet" with mulitvitamin (zinc) and antioxidants (smoking cessation) wet: rapid loss of vision due to secondary bleeding of choroidal neovascularization Due to hypoxia Treat with anti-VEGF (Ranibizumab and pryaptanib) or laser