week 3- neuro 2 Flashcards

1
Q

• Seizure Disorder, terms, etio:

A

o Sz: abnormal, unregulated electrical discharge in brain’s cortical gray matter, transiently interrupts normal brain fxn → altered awareness, abn sensations, focal involuntary movements, convulsions (widespread violent involuntary contraction of voluntary muscles).
o Epilepsy: Common, mb serious neuro do; recurrent, unprovoked szs. st idiopathic, or various malformations, strokes, tumors can cause
o Nonepileptic szs: dt temporary do: Metabolic do, CNS infx, Drug toxicity or w/d
o Symptomatic sz: dt known cause (brain tumor or stroke)
o Psychogenic sz (aka Pseudoseizure): No electrical discharge in brain
o Etio: AI dos, Cerebral edema, Head trauma, CNS infx, Congenital or Developmental abn, Drugs or toxins, Expanding intracranial lesions, Hyperpyrexia (↑ fever), Metabolic disturbances, Pressure related, W/d syndromes

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2
Q

• Generalized Seizures, types:

A
o	Electrical discharge in entire cortex of both hemispheres; Complete LOC; usu dt metabolic disturbances
o	Infantile spasms
o	Absence seizures (aka Petit Mal)
o	Tonic-clonic seizures (aka Grand Mal)
o	Atonic seizures
o	Myoclonic seizures
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3
Q

• Infantile spasms

A

o Sudden flexion and adduction of arms with forward flexion of trunk
o few seconds, many x/d
o only in 1st 5 yrs, usu replaced by other seizure types

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4
Q

• Absence seizures (aka Petit Mal):

A

o Typical: ages 4-12; FHx in 40%; mb many x/d, 5-30 sec. st LOC, eyelid fluttering; stares vacantly, abruptly stop/resume activity; No falling or convulsing; usu sitting, mb preceded by hyperventilation. Rare with exercise. Usu normal Neuro and cognitive exams
o Atypical: usu part of Lennox-Gastaut syndrome (severe begins under 4) Last longer. Complete LOC. usu hx of damage to nervous system, szs continue into adulthood

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5
Q

• Tonic-clonic seizures (aka Grand Mal)

A

o Primary: Begin wi outcry → LOC and falling→ tonic contraction →clonic motion of muscles of head, extremities, trunk. St: Urinary or fecal incontinence, Tongue biting, Frothing at mouth, Usu 1-2 min, No aura
o Secondary: Begin w simple partial or complex partial seizure that generalizes; May have all the sxs as above except usu. no outcry

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6
Q

• Atonic, myoclonic seizures

A

o A: usu children (Lennox-Gastaut); Brief complete loss of muscle tone, LOC; Often fall to ground: risk head injury or trauma
o M: Brief, lightening-like jerks of a limb, several limbs or trunk; mb repetitive; UL or BL. Unlike other BL szs, no LOC unless progresses into general tonic-clonic sz

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7
Q

• Partial Seizures (as opposed to generalized), types:

A

o Excess neuronal discharge in one cerebral cortex; Often from structural abnormalities
o Simple
o Complex

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8
Q

• Simple Partial, types:

A

o Cause motor, sensory, or psychomotor sxs without LOC
o Types: MOTOR AND SENSORY SEIZURES INDICATE STRUCTURAL BRAIN DISEASE, THE FOCAL ONSET LOCALIZING THE LESION: FULL INVESTIGATION IS MANDATORY!!!!
o Motor: Arise in frontal motor cortex, movts in contralateral face, trunk or limbs; clonic (shaking), usu begins in hand or face (largest representative cortical area); Jacksonian motor seizure (aka Jacksonian March): A “march” of involuntary muscle movt from one muscle group to next
o Sensory: Arise in sensory cortex; Parasthesias or tingling in extremity or face st assoc w distortion of body image; Visual, Auditory and Autonomic  all RARE

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9
Q

• Complex Partial

A

o reduced but not complete LOC; Usu in temporal lobe, w aura; stare; Consciousness impaired, some awareness of environment (may withdraw from noxious stimuli)
o Automatisms: Oral: involuntary chewing or lip smacking; Limbs: often purposeless movs of hands; if ambulatory, may wander off
o Head or eye deviation to contralateral side
o Motor sxs 1-2 min. Confusion 1-2hr

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10
Q

• Ssx of seizures

A

o mb preceded by aura
o usu end in 1-2 min
o Generalized seizures followed by postictal state: Deep sleep, HA, Confusion, Muscle soreness
o Sometimes Todd’s paralysis after partial motor seizure (transient neuro deficit, usu weakness of CL limb)

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11
Q

• Hx for seizures

A

o sxs (aura?), duration?
o Ask family members or witnesses
o Risk factors: head trauma or CNS infx, Known neuro do; Drug use or w/d (esp recreational); Alcohol w/d; Non-adherence to anticonvulsants; FHx seizures or neuro dos
o Rare triggers: Repetitive sounds, Flashing lights, Video games, Touching certain body part, Sleep deprivation

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12
Q

• PE, work-up, px for seizures:

A

o PE: mb bitten tongue, soiled clothing (incontinence), prolonged confusion; Fever and stiff neck?- Meningitis or encephalitis; Papilledema?- ↑intracranial pressure
o Labs: CBC, CMP (w glucose), LFTs, Tox screen, Lumbar puncture (if infx suspected but usu. CT brain first)
o Imaging: CT to exclude mass or hemorrhage; Follow-up MRI Recommended when CT is (-); EEG Critical for Dx but normal EEG cannot necessarily r/o seizure do
o Px: With tx: szs eliminated in 1/3 of pts; 1/3 frequency ↓ > 50%; 60% well-controlled by meds can eventually stop meds, remain sz free

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13
Q

• Brain Abscess, etio, ssx, dx::

A

o intracerebral collection of pus
o Etio: cranial infx (osteomyelitis, mastoiditis, sinusitis, subdural empyema); head wound; Hematogenous
o Ssx: HA, N/V, lethargy, fever, Focal neuro deficits, szs
o Dx: CT or MRI

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14
Q

• Encephalitis:

A

o inflam parenchyma of brain
o Etio: direct viral invasion; In US: Mosquito-borne arboviral encephalitides: infect when weather is warm (spring, summer, fall); mc sporadic: HSV; HIV
o At risk: Children, Elderly, weak immune systems
o Ssx: Fever, HA, Altered mental status, szs, Focal neuro deficits
o Dx: MRI, CSF testing (w HSV will show ↑ WBCs, esp lymphocytes; Suspect w unexplained alterations in mental status
o Px: Recovery mb very long; Permanent neuro deficits common if survive severe infx

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15
Q

• Rabies:

A

o viral encephalitis transmitted by saliva of infected bats and other select mammals
o ssx: Depression, Fever, Agitation, Excessive salivation, Hydrophobia
o dx: Suspect w encephalitis or ascending paralysis, recent hx animal bite or exposure to bats; Skin bx; St PCR of fluid or tissue samples

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16
Q

• Helminthic Brain Infections:

A

o parasitic worms infx CNS
o millions of ppl in developing countries, mb travelers or recent immigrants
o In Western Hemisphere: mc pork tapeworm (taenia solium)
o Ssx: encephalitis, meningitis, cerebral masses, hydrocephalus, myelopathy

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17
Q

• Progressive Multifocal Leukoencephalopathy

A

o Etio: reactivation of JC virus usu pts. w impaired cell-mediated immunity (HIV)
o Path: demyelinating dz; esp affects parietal and temporal lobes
o Ssx: Clumsiness mb 1st sx, Hemiparesis mc; Aphasia, dysarthria, hemianopia
o Dx: MRI (Multifocal, non-enhancing lesions w/o mass effcct), CSF: look for JC virus DNA w PCR; Brain bx st for definitive Dx

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18
Q

• Subdural Empyema:

A

o collection of pus bw dura mater and arachnoid
o Etio: Usu complication of sinusitis, Ear infx, Cranial trauma, Rarely bacteremia
o Ssx: Fever, Lethargy, Focal neuro deficit, sz
o Dx: MRI

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19
Q

• Prion dz (Transmissible Spongioform Encephalopathies):

A

o Progressive, fatal, untreatable brain dos
o rare; worldwide: 1 in 1,000,0000
o Transmission: hereditary, sporadic, transmitted (person to person w kuru, or animal to person w CJD)
o Path: misfolding of normal cell- surface brain protein (prion protein, PrP), exact function is unknown

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20
Q

• Creutzfeldt-Jakob Disease (CJD):

A

o sporadic, familial or acquired: Sporadic (sCJD) 85%; Variant (vCJD) dt eating meat from cattle with bovine spongioform encephalopathy (BSE; aka Mad Cow Dz); usu > 40yr (avg 60)
o Ssx: Memory loss, Confusion; Incoordination, ataxia; Startle myoclonus (provoked by noise, etc)
o Dx: Suspect in elderly w rapidly progressing dementia esp w ataxia or myoclonus; MRI
o Px: Death usu in 6-12 mos; life expectancy for vCJD is longer (avg 1.5 yrs)

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21
Q

• Other types of prion dzs:

A

o Variably Protease Sensitive Prionopathy (VPSPr)
o Gerstmann-Sträussler-Scheinker Disease: Similar to CJD, much less common; familial (AD); earlier age than CJD, longer life span
o Fatal Insomnia: Rare hereditary or sporadic; onset usu 40; difficulty sleeping, motor dysfunction, death
o Kuru: in Papua New Guinea, spread from man to man thru cannibalism

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22
Q

• Meningitis:

A

o Inflam meninges and subarachnoid space; dt infx, other do or rxn to drugs
o Ssx: HA, fever, nuchal rigidity (seen in all types)
o PE: (+) Kernig, (+)Brudzinski; difficulty touching chin to chest with mouth closed; difficulty touching forehead or chin to knee
o Dx: CSF; MRI 1st if ssx of ↑ intracranial P, to avoid brain herniation in addition to blood cultures

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23
Q

• Acute Bacterial Meningitis

A

o rapidly progressing bacterial infx of meninges and subarachnoid space
o Path: Hematogenous spread; Nearby infx structures: sinuses, middle ear; Congenital or acquired defect in skull (penetrating head wound, surgery, etc.)
o Mc etio: Children (Neisseria meningitidis, Streptococcus pneumoniae), Middle age and elderly (Strep Pneumoniae)
o Ssx: 3-5 d progressive non-specific sxs: malaise, fever, irritability, vomiting, tachycardia, HA, photophobia, changes in mental status (lethargy, obtundation), nuchal rigidity (not all pts), st back pain, szs in 40% children
o Dx: CSF (↑WBCs (usu. PMNs), protein, ↓ glucose), CBC with diff, CMP, Blood culture
o Mortality: 60

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24
Q

• Viral Meningitis:

A

o Less severe than bacterial
o Mc dt Enteroviruses; also HSV
o Ssx: 1st Fever, Myalgia, GI or Resp sxs; then HA, fever, nuchal rigidity
o Dx: CSF: Protein slightly ↑ but less than in bacterial; Glucose usu normal or ↓ slightly; ↑ WBCs (lymphocytes)

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25
Q

• Noninfectious Meningitis

A

o less severe than acute bacterial
o dt Noninfectious Dos: Metastatic CA, Sarcoidosis, Behçet syndrome, SLE, Sjögren RA, Rupture of intracranial cysticercal or epidermoid cyst, Drugs, Vaccines
o ssx: typical
o dx: sterile CSF (no sign infx)

26
Q

• Recurrent Meningitis

A

o dt bacteria, virus, or noninfectious; mc HSV
o HSV:  3 episodes fever, nuchal rigidity, and CSF with ↑ lymph; episodes last 2-5 d, resolve spontaneously
o bacteril: suspect congenital or acquired defect of spine or skull that has not been corrected
o Drugs: causative agent is used again accidently or intentionally

27
Q

• Subacute and Chronic Meningitis

A

o Subacute: Develops over d-wks
o Chronic: last > 4wks
o Possible Causes: Fungi, Mycobacterium tuberculosis, Rickettsiae, Spirochetes, Toxoplasma gondii, HIV, Enteroviruses, AI or rheumatic dos (eg, SLE, RA), CA
o Dx: Clinical findings non-specific; mb not dx w CSF, mb need more invasive testing; Cisternal or ventricular puncture, bx

28
Q

• Tremor:

A

o Involuntary, rhythmic movement of any body part dt contraction of agonist/antagonist muscle groups
o Most prevalent movt do
o Pathogenesis: unclear
o Physiologic (normal): Evident on maintaining a fixed posture, Fast in rate; Enhanced by fatigue, anxiety, drugs; Non-disabling
o Pathologic: at rest or w movt, Slow in rate, Coarse in character, Socially and physically disabling; Resting: occur when body part is fully supported against gravity; Action: occur during motion

29
Q

• Essential Tremor

A

o Not benign or essential; FHx in 50%
o 20x MC than PD
o Ssx: w voluntary movt (action tremor; Parkinsonian is at rest)
o Usu BL
o Can worsen with age and interfere with normal activity
o Alcohol alleviates sxs, reduces overactivity of cerebellum (alcoholism may result)

30
Q

• Hx for tremor:

A

o Onset? Agg. factors? Body parts affected?
o ROS: Recent weight loss, ↓ appetite, diarrhea, palpitations, heat intolerance (hyperthyroid); Muscle rigidity, gait and postural problems, slow movt (Parkinsonism); Sudden onset of motor weakness, dysarthria (stroke), etc
o FHx: Essential tremor? Other neuro dz?
o SHx: Meds and drugs

31
Q

• PE for tremor, Red flags:

A

o PE: Vitals, HEENT: exopthalmus or eyelid lag? Thyroid, Cardio, Extensive neuro exam: Esp have pt extend arms out in front, look for tremor; try spiral hand drawings for documentation
o RF: Abrupt onset;

32
Q

• Fragile X-Associated Tremor/Ataxia Syndrome (FXTAS)

A

o Genetic, usu men; tremor, ataxia and dementia; People with the permutation are considered carriers
o mc form of intellectual disability in males, develops when the mutation is full ( > 200 repeats)
o Ssx (become noticeable in late adulthood): Intention tremor, Ataxia, Parkinsonism, Neuropathy, dysautonomia
o Dx: Genetic testing

33
Q

• Huntington disease:

A

o inherited, AD → progressive, selective (localized) neural cell death, w choreic movts and dementia; onset 35-40; 4-7/100,000
o Path: neuronal loss in basal ganglia
o Ssx: Dementia or Psych disturbances can form before movt dos; Chorea (uncontrollable twisting and writhing movements); Tics; Myoclonal disturbances; Typical features: Bizarre, puppet-like gait, Facial grimacing, Inability to intentionally move eyes quickly
o Dx: Clinical eval confirmed by genetic testing; Neuroimaging may help identify caudate atrophy and some frontal predominant cortical atrophy

34
Q

• Parkinson disease, etio, incidence:

A

o Idiopathic neurodegenerative do characterized by bradykinesia, resting tremor, cogwheel rigidity, postural reflex impairment
o very common neuro do
o Typical onset 40-70yrs; M:F 3:2
o Patho: loss of pigmented DA neurons in substantia nigra; presence of Lewy bodies (eosinophilic cytoplasmic inclusions in pigmented neurons)
o Etio: Genetic predisposition likely (~10% have FHx); mb Environmental factors (Smoking, Herbicides, CO, Manganese, Carbon Disulfide); Oxidative stress (↓ glutathione in brain?)

35
Q

• PD ssx, dx

A

o Ssx: Mask-like facies; Coarse tremor (pill-rolling tremor); usu. starts in 1 limb UL, spread eventually to all 4 (at rest, improves w movt and sleep); Rigidity: mostly flexor muscles of neck, trunk, limbs → flexed posture; Bradykinesia; Shuffling gate; Postural instability → falls; Dementia in 30%
o Dx: Mainly clinical: UL resting tremor that disappears (or attenuates) during finger-to-nose coordination test; On exam cannot perform rapid alt movts; Sensation and strength usu normal; Reflexes normal, mb difficult to elicit dt rigidity
o Often clinicians test trial of levodopa to distinguish PD from 2nd or atypical Parkinsonism. large sustained response suggests Parkinsonism /PD; no response suggests sxs dt another cause

36
Q

• Tic Disorders:

A

o Rapid, repetitive movts, erupt spontaneously from background of normal motor activity
o Can be motor or phonemic

37
Q

• Tourette Syndrome:

A

o motor and vocal tics; Onset in childhood; M > F; mb hereditary; mb DA system in basal ganglia
o Criteria for Dx: Multiple motor and 1+ phonemic tics; many x/d; Onset

38
Q

• Restless Legs Syndrome:

A

o Ssx: Irresistible urge to move legs, arms, st other body parts usu w paresthesias (creeping or crawling sensations); Sxs more prominent during inactivity, peak at bedtime; To relieve sxs, pts. kick, move, toss extremity → difficulty sleeping
o Etio: Idiopathic, mb related to abn DA transmission in CNS
o Dx: hx alone, Important to r/o other possible causes with labs: CBC (anemia), Ferritin (↓ iron storage), CMP (LV and KD fxn)

39
Q

• Multiple Sclerosis, etio, incidence, path:

A

o disseminated patches of demyelination in brain and spinal cord
o Etio: immunologic mechanism (EBV?), Genetic susceptibility; mc in pppl who spend first 15 years of life in temperate climates rather than tropics (Lower vit D?), Cigarette smoking ↑risk
o F > M, onset 15-60, usu 20-40
o Path: Destruction of oligodendroglia → demyelination; Cell bodies and axons usu not damaged

40
Q

• Ssx of MS:

A

o mc initial sxs: Paresthesias in 1+ extremities, trunk, one side of face; Weakness or clumsiness of leg or hand; Visual disturbances (eg, partial loss of vision and pain in one eye dt retrobulbar optic neuritis, diplopia dt ocular palsy, scotomas)
o Other Common Sxs: Slight stiffness or easy fatigability of a limb; Minor gait disturbances; Urinary incontinence; Vertigo; Excess heat can exacerbate sxs

41
Q

• Typical Clinical Course of MS:

A

o Relapsing-Remitting Pattern: usu early in course; Exacerbations alt w remissions; Remissions can last mos-yrs; relapse spontaneously or triggered by infx
o Primary Progressive Pattern: progresses rapidly w/o remission
o Secondary Progressive Pattern: Initially begins w relapsing-remitting course → progressive
o Progressive Relapsing Pattern: rare; progresses gradually w sudden relapses

42
Q

• PE for MS:

A

o HEENT: Central scotoma, Temporal pallor in optic disc, Opthalmoplegia
o Neuro: Wide-based gait, Spastic gait, Reflexes: exaggerated repetitive knee jerk, Loss of position sense, Neurogenic bladder, cannot run heel down shin evenly, Intention tremor, Finger-to-nose test failed w closed eyes

43
Q

• Dx of MS, px:

A

o Clinical criteria: Hx of exacerbations and remissions; Objective demonstration on exam or test of > 2 neuro abn
o MRI of brain and spinal cord: Most sensitive test for MS, many plaques, but # does not correlate with sx/dz severity
o CSF: IgG usu ↑, mb ↑ Total protein
o Other tests: Visual evoked potential: help determine optic nerve involvement; Somatosensory evoked potential: may detect central sensory pathway lesions
o Px: variable

44
Q

• Neuromyelitis Optica

A

o Affects only eye and spinal cord
o Acute optic neuritis st BL plus demyelination of cervical and thoracic spinal cord
o Previously considered a variant of MS, now = different do
o Ssx: Visual loss, Paraparesis or quadraparesis, Incontinence
o Dx: Brain and spinal cord MRI, Visual evoked potentials

45
Q

• Peripheral Nervous System and Motor Unit Disorders

A

o Peripheral Nervous System: part of nervous system outside brain and spinal cord
o Motor Unit: consists of anterior horn cell, motor axon and muscle it innervates
o Nerve fibers outside spinal cord join to form anterior (motor) and posterior (sensory) nerve roots

46
Q

• Disorders of Neuromuscular Transmission

A

o May affect: Presynaptic neuron- Affects release of ACh (botulism)
o Breakdown of ACh in synapse: dt drugs or neurotoxic chemicals
o Postsynaptic receptor: For example: Myasthenia Gravis

47
Q

• Myasthenia Gravis

A

o episodic muscle weakness and easy fatigability dt immune destruction of ACh receptors
o usu F 20-40; If gives birth, infant may develop neonatal myasthenia (12%) dt IgG Abs that cross placenta
o Ssx: Fatigability (Muscle weakness w use); Weakness resolves with rest; Eyes: Ptosis, Diplopia; Oropharyngeal: Dysphagia, Dysarthria: Resp: Recurrent pneumonia, Pulmonary failure

48
Q

• MG dx:

A

o Suggested by hx and PE
o Bedside tests: Tensilon: only in w obvious ptosis or opthalmoparesis; IV Tensilonto observe if dramatic improvement in muscle weakness
o Ice-pack test: w ptosis who Tensilon may be too risky for; Based on physiologic principle of improved neuromuscular transmission at ↓ temp; Ice pack on lid for 2 mins, then removed and effect on ptosis immediately observed
o Confirmed by: Serum Anti-AchR Abs; EMG
o Once MG dx: CT or MRI of thymus to check for thymoma (assoc w MG)

49
Q

• Guillain-Barré Syndrome (GBS) (Acute Idiopathic Polyneuritis; Acute Inflammatory Demyelinating Polyradiculopathy):

A

o mc acquired inflam neuropathy
o Cause: not fully understood; mb AI
o Ab and cell-mediated reactions to peripheral nerve myelin
o In 2/3 of pts. sxs begin 5 d – 3 wks after infx, surgery or vaccination
o Infx is trigger in 50%
o Campylobacter jejuni, enteric viruses, herpes viruses (including CMV and EBV), and Mycoplasma spp

50
Q

• GBS ssx:

A

o motor impairment > sensory
o Sensory sxs to begin: parasthesia of feet then hands
o Then, Rapid onset severe muscle weakness esp. soon after surgery, infx, or vaccination
o Usu. weakness is symmetric, begins w legs, progresses to arms
o Weakness is maximal at 3 wks
o Facial muscles can be weak
o Sphincters usu spared
o Mb Respiratory paralysis
o At its worst: total flaccid quadriplegia

51
Q

• PE, dx, course, ddx, px for GBS:

A

o PE: mb autonomic dysregulation (Sinus tachycardia, Urinary retention); Test for subtle proximal and distal strength: rise from a chair, Step up on step, Kneel on one knee and stand, Walk on heels and then toes; DTRs are lost
o Dx: Clinical, Electro-dx testing, CSF analysis (↑ protein)
o Course: 50-90% recover completely, mb some residual weakness or AbN sensation like numbness or tingling
o Ddx: Myasthenia Gravis: weakness, early ptosis, opthalmoplegia; DTRs are retained; MS: doesn’t resolve; hyperreflexia; DM: glove and stocking parasthesias but DTRs retained; ↑ Glucose
o Px: Fatal in

52
Q

• Amyotrophic Lateral Sclerosis (ALS) and Other Motor Neuron Diseases (MND):

A

o UMN or LMN features or both
o UMN: Affect neurons of motor cortex which extend to brain stem (corticobulbar tracts) or spinal cord (corticospinal); Sxs: stiffness, clumsiness, awkward movts; usu affecting mouth, throat, then spread to limbs
o LMN: Affect anterior horn cells, cranial nerve motor nuclei, or their efferent axons in skeletal muscle; Sxs: CNs affected: facial weakness, dysphagia, dysarthria; Anterior horn cells affected: muscle weakness and atrophy, fasciculations (visible muscle twitches), muscle cramps (initially in hand, foot, tongue)

53
Q

• ALS, etio, ssx:

A

o (aka Lou Gehrig’s disease) is MC MND; May involve CNS, part of PNS; 1-3/100,000
o Onset: middle and late life (avg 55); M > F until 65, then equal
o Etio: Sporadic mc (unknown etio); Familial less common
o Random, asymmetric sxs: cramps, weakness, muscle atrophy of hands and feet; Weakness progresses to forearms, shoulders, lower limbs; Fasciculations, spasticity, hyperactive DTRs; Awkwardness with movts; Difficulty controlling facial expressions or tongue movts; Hoarseness; Dysphagia; Slurred speech; Mind remains intact, no deterioration of mental ability

54
Q

• ALS PE, px, dx, ddx

A

o PE: weight loss; Neuro: Fasciculations and spasticity of muscles, Hyperactive DTRs, (+) Babinski (aka Extensor plantar reflex); Extremities: Wasting in hand (“skeleton hand”)
o Px: Poor; death in 3yr in > 50%; Death usu dt resp failure
o Dx Clinical Criteria (requires both UMN and LMN dos in multiple areas to be classified as ALS): Basic labs to r/o other dos, Electro-dx tests, MRI of brain or cervical spine (usu normal), CSF
o Ddx: Dos of neuromuscular transmission, Various myopathies, Polymyositis, Dermatomyositis, Thyroid and adrenal dos, Electrolyte abn

55
Q

• Intracranial and Spinal Tumors

A

o Primary: originate in brain parenchyma or extraneural structure
o Secondary: dt metastasis (10x mc than primary)
o Ssx: HAs, Esp. new onset of persistent, unexplained HA worse w sleep; Deterioration in mental status; Focal brain dysfunction; Evidence of ↑intracranial pP (vomiting, papilledema); New szs
o Dx: MRI or CT

56
Q

• Gliomas

A

o Primary tumors originate in brain parenchyma
o Astrocytomas (mc glioma): Tend to develop in younger patients
o Oligodendrogliomas (most benign): Affect mainly cerebral cortex
o Medulloblastomas and ependymomas: Usu. develop near 4th ventricle; both tend to cause obstructive hydrocephalus
o Medulloblastoma usu affects children and young adults
o Ependymomas (uncommon) mainly in children

57
Q

• Meningiomas

A

o Benign tumors of meninges, can compress adjacent brain tissue
o a more common brain tumors
o Only brain tumor w F > M
o usu 40-60, or younger

58
Q

• Pineal Region Tumors

A

o usu during childhood
o mb ↑ intracranial P by compressing aqueduct of Sylvius
o May also cause: paresis of upward gaze, ptosis and loss of papillary light accommodation reflexes
o May cause precocious puberty b/c hypothalamus is compressed

59
Q

• Pituitary Tumors

A

o Most are adenomas
o Ssx: HA, Visual manifestations, Endocrinopathies
o Dx: MRI

60
Q

• Primary Brain Lymphomas

A

o Originate in neural tissue; usu B-cell tumors

o Dx: MRI; Sometimes CSF or biopsy

61
Q

• Intracranial/Spinal Cord Tumors

A

o Develop inside or outside spinal cord parenchyma and may directly destroy tissue or compress cord or nerve roots
o Ssx: Progressive back pain (Unrelated to activity and worsened by recumbency) Neurologic deficits
o Dx: MRI