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  1. Corticospinal (pyramidal) Tract
    • Voluntary movement
    • Complicated/delicate movements
    • Slight tension (when muscle is relaxed)
  2. Corticobulbar Tract
    Cranial Nerves movements
  3. Basal Ganglia System
    • Muscle tone
    • Controls gross autonomic mvts (walking)
  4. Cerebellar System
    • Maintains equilibrium
    • Controls posture
  5. Spinothalamic Tract
    • Pain
    • Temp
    • Crude Touch
  6. Posterior Columns
    • Vibration
    • Proprioception
    • Pressure
    • Fine touch
  7. Upper Motor Neurons: (UMN)
    nerve cell bodies
  8. umn
    Located in the motor strip of the cerebral cortex and in several brainstem nuclei
  9. UMN synapses
    synapse with motor nuclei in brainstem (cranial nerves) and spinal cord (peripheral nerves)
  10. UMN crossover
    tracts crossover in the medulla of the brainstem and carry impulses to spinal nerves
  11. umn damage above crossover
    motor impairment develops on the contralateral side
  12. umn damage below crossover
    motor impairment develops on the ipsilateral side
  13. Lower Motor Neurons: (LMN)
    • or cell bodies are called anterior horn cells
    • LMN
    • transmit impulses through anterior roots and spinal nerves to peripheral nerves which terminate at the neuromuscular junction
    • Damage to LMN
    • causes ipsilateral weakness and paralysis,
    • decreased muscle tone
    • and decreased or absent reflexes
  14. Anterior Circulation:
    70% of strokes occur anteriorly (anterior arteries in the Circle of Willis)
  15. Internal Carotid Artery
    - progressive stuttering onset, weakness on contralateral side, numbness/paresthesias, gaze deviation toward infarcted hemisphere, Horner’s syndrome affected side, reflex changes, lethargy, stupor
  16. Anterior Cerebral Artery:
    • paralysis and decreased sensory of opposite leg and arm, apraxia, decreased opposite grasp reflex, absent spontaneity
    • Anterior Communicating Artery
  17. Middle Cerebral Artery: p
    aralysis and decreased sensory of opposite arm weaker than leg, aphasia, agraphia, apraxia, confusion, gaze toward infarcted hemisphere
  18. Posterior Circulation strokes
    30% of strokes occur posteriorly
  19. Vertebral Artery and Basilar Artery
    • Cranial nerve palsies, diplopia, vertigo,
    • nausea/vomiting, dysarthria, perioral weakness,
    • dysphagia,
    • ipsilateral facial sensory and motor loss,
    • contralateral hemiparesis, impaired consciousness, coma
  20. Posterior Cerebral Artery
    • homonymous hemianopsia,
    • memory deficit, visual hallucinations,
    • sensory loss,
    • CNIII palsy, paralysis of eye movements,
    • contralateral hemiplegia, ataxia
  21. Transient Ischemic Attack: (TIA)
    • sudden, focal ischemia causing transient neurological deficits
    • 80% usually last a couple of mins., but no more than 24 hr , resolves completely
  22. TIA Risk
    • increases with age
    • male > female
    • called “warning sign” of impending stroke
  23. TIA Etiology
    • Embolism causing interruption of blood flow to certain part of brain
    • cardia
    • Non cardiac
  24. TIA etiology Cardiac
    Afib, rheumatic dz, valvular dz, infective endocarditis
  25. TIA etiology Non-Cardiac
    atherosclerosis, inflammatory, lesions/tumor, polycythemia, sickle cell dz
  26. TIA Risk stratification:
    ABCD2 - age, BP, Clinical features, duration, DM (3 or more admit)
  27. TIA Diagnostic Studies:
    • MRI (within 24hr of symptoms),
    • CBC, CMP, lipid panel, cardiac enzymes, coags,
    • consider carotid Doppler,
    • CT angio,
    • Cerebral arteriography (gold standard diagnostic and theraputic)
  28. TIA Treatment
    Goal to prevent stroke.
  29. TIA TX Non-cardioembolic:
    Anti-platelet – ASA, clopidogrel (Plavix), ASA/Dipyridamole (Aggrenox), Cilostizol (Pletal)
  30. TIA tx Cardioembolic
    warfarin (Coumadin)
  31. TIA Modify risk factors
    • control DM, control HTN, statins for hyperlipidemia, smoking cessation, healthy diet and exercise
    • Surgery for focal carotid stenosis of >70-98%
  32. Stroke = Cerebral Vascular Accident (CVA)
    • Ischemic and Hemorrhagic
    • Abrupt/sudden onset, cell death due to inadequate blood flow in localized area, hemiparesis or monoparesis, sensory deficits, visual fields deficits, vision loss, diplopia, dysarthria or aphasia, ataxia, facial droop, nystagmus, decrease in level of consciousness
  33. Ischemic :
    • caused by thrombotic or embolic
    • Lacunar or Small-vessel (usually associated with uncontrolled HTN)
    • Carotid or Large-artery (vertebrobasilar, cerebral arteries)
    • Cardioembolic infarction (source of recurrent strokes)
  34. Ischemic cva Risk Factors
    • prior TIA/stroke, HTN, DM, hypercholesterolemia,
    • increased blood viscosity, smoking,
    • FH stroke, cardiac (rhythm, valve, muscle dz),
    • excess alcohol
  35. Ischemic Stroke assess
    good history and PE, (serial neuro exams) determine time frame/onset of symptoms, determine ischemic vs hemorrhagic, rule out trauma, NIHSS
  36. ischemic Diagnostic studies:
    • CT = quick, evaluate acute bleed vs ischemic (90-95% sensitive SAH)
    • MRI = takes time to get, good when looking for tissue changes (poor with hemorrhages)
    • CBC, CMP, ECG, CXR, LP if suspect hemorrhage and imaging inconclusive, Blood cx if suspect infection, coags, cardiac enzymes
    • Echocardiogram rule out valvular dz.
  37. Ischemic Treatment:
    • ABC’s, supplemental oxygen, airway management,
    • fibrinolytic therapy/antiplatelet agents,
    • glycemic control, optimal blood pressure control
  38. Ischemic Stroke tPA therapy –
    Given within 3 hours (4.5 hours) of stroke onset, given only after CT scan ruled out hemorrhagic stroke, should be given within 1 hour after arriving to the hospital, 18 yrs or older, do not give if >4.5 hours after onset of ischemic symptoms
  39. Contraindications to tPA
    Head trauma or prior stroke in previous 3 months, symptoms suggestive of subarachnoid hemorrhage, history of intracranial neoplasm, arteriovenous malformation, or aneurysm, recent intracranial or intraspinal surgery, increased risk for hemorrhage (anticoag meds INR>1.7), systolic BP >185 mmHg, diastolic BP > 110 mmHg
  40. If patient not a candidate for tPA
    • inpatient in stroke unit if available, monitor O2, treat BP >185/110, prevent hyperthermia, early ambulation/PT, SC heparin, if surgical candidate carotid endarterectomy if stenosis >70%,
    • Medical management = ASA 325 mg daily, Warfarin – target INR 2-3
  41. Hemorrhagic Stroke:
    less common than ischemic (15% of all strokes)
  42. Intracerebral Hemorrhage (ICH) stroke
    10% of bleeds)
  43. Ich Risk factors:
    HTN, noncompliance with meds, smoking, excess EtOH, younger than 55 yo
  44. Ich Causes
    Intracranial aneurysms, AVM’s, neoplasms, coagulopathy (Coumadin), drugs (cocaine), HTN, ischemic infarction, Cerebral Venous Thrombosis
  45. ICH Signs/symptoms:
    sudden, severe HA, then obtunded, marked elevated BP, maximum deficit at onset
  46. Subarachnoid Hemorrhage (SAH):
    (5% of bleeds)
  47. SAH Risk factor
    for aneurysm rupture is smoking
  48. SAH Causes:
    • Trauma = 80% related to head injury
    • Spontaneous = 20% related to aneurysms (in 40-70 yo) or AVM’s (in 20-40 yo)
  49. SAH Signs/symptoms:
    • immediate severe headache “Worst headache of my life”, Thunderclap HA
    • May have symptoms (sentinel event) in previous 30 days = warning leaks
    • Photophobia
    • N/V
    • +/- focal neuro deficits
    • +/- LOC
  50. ICH and SAH work up:
    • Good history
    • Labs: CBC, coags, CMP, ESR, toxicology
    • LP: xanthochromia (yellowish color indicating bilirubin from breakdown of blood)
  51. Hemoragich stroke Imaging
    • CT = bleed/hemorrhage/hydrocephalus in first 24 hours
    • MRI = ischemia, structural changes
    • Cerebral angiography = identify source of bleed –
    • ~~gold standard for surgical evaluation(pre-op)
    • CT – bleed shows immediately
  52. Hemorrhagic Stroke Treatment:
    • directed to prevent re-bleed, hydrocephalus and cerebral vasospasm
    • Manage: ABC’s, BP, fever, blood glucose level, electrolytes, agitation/seizures, intracranial pressure
  53. Hemorrhagic stroke Surgical measures:
    • obliterate AVM’s - surgical removal or balloon, sclerosing agents, embolization
    • obliterate aneurysm - surgical clipping, endovascular balloon angioplasty
    • Treat hydrocephalus: surgical shunt placement
  54. Subdural hematoma:
    • bleed between dura and arachnoid membrane, common after trauma
    • Presents with HA and confusion (patient can be lucid after impact and prior to symptoms developing)
    • Concave lesion on CT scan, monitor with serial CT’s (worsening symptoms), supportive care, surgery in severe cases

    • Dementia
    • Progressive decline in intellectual function
    • Usually an insidious onset with gradual progression
    • Typically begins after age 60 (more prevalent in women because of longer life expectancy)
    • Most common cause is primary neurodegenerative disease
  55. Most common cause of dementia
    Primary neurodegenerative disease
  56. Dementia Risk factors
    • Family history of dementia
    • DM
    • Vascular disease (ie stroke)
    • History of significant head injury
    • Smoking (2-4 fold increase)
  57. Dementia Sign/Symptoms:
    • Short term memory loss
    • Word finding difficulty
    • Visuospatial dysfunction
    • Executive dysfunction
    • Apathy
    • Apraxia
  58. Short-term memory loss:
    • results from pathology in the hippocampus
    • Repeating questions or stories
    • Diminished ability to recall details of recent conversations/events
  59. Word finding difficulty:
    • results from pathology in the temporoparietal jn left hemisphere
    • Difficulty recalling names of people, places, objects
    • Low-frequency words affected first – speak in a round-about-way, indirect way
  60. Visuospatial Dysfunction:
    • results from pathology in right parietal lobe
    • Poor navigation, getting lost in familiar places
    • Impaired recognition of familiar faces
  61. Executive Dysfunction
    • results in pathology in various areas; frontal lobe or basal ganglia or cerebral white matter
    • Easy distractibility and Impulsivity
    • Slowed processing speed
    • Poor planning/organization
  62. Apathy:
    • results in pathology of frontal lobe or basal ganglia or cerebral wht. matter
    • Indifference, separate from depression
  63. Apraxia:
    • results from pathology of frontal or parietal lobes especially left parietal
    • Loss of learned motor behaviors
  64. Pathology of frontal lobe or basal ganglia or cerebral white mater
    • Executive dysfunction
    • Apathy
  65. Right parietal lobe pathology
    Visuospatial dysfunction
  66. Front or L parietal lobe
  67. Left temporoparetal pathology
    Difficulty finding words
  68. Hippocampus pathology
    Short term memory loss
  69. Dementia r/o
    • new cognitive complaints
    • – rule out cerebrovascular disease, tumor, other possible causes of decreased cognition
  70. Dementia imaging
    • MRI is preferred – evaluate for global or focal brain atrophy
    • CT without contrast if MRI not available
    • PET scan – with fluoro-deoxyglucose can help discriminate between Alzheimer’s and Frontotemporal pathology (but less sensitive after age 60-70)
  71. Dementia Labs
    B12, TSH/T4, RPR (if risk or suspicion of syphilis), CBC, CMP(glucose, electrolytes)
  72. Dementia Differential Diagnosis:
    • Age related demntia (90%)
    • Other
  73. Common age related dementia:
    • (90%)
    • Alzheimer’s disease
    • Vascular dementia
    • Dementia with Lewy Bodies (DLB)
    • Frontotemporal dementia (FTD)
  74. Other causes of dementia
    • (10%)
    • Brain tumor
    • Drug reactions
    • Alcoholism / other addictions
    • Depression
    • Nutritional deficiencies
  75. Frontotemporal Dementia (FTD):
    • Age at peak incidence in 60’s
    • Prominent behavioral and personality changes:
    • RELATIVE PRESERVATION OF MEMORY (different from Alzheimer’s)
    • Associated with ALS
  76. Ftd BEHvioral/personality changes
    • Deficits in empathy, insight, executive function
    • Disinhibited, impulsive behavior
    • Hyperorality (inappropriate objects into mouth)
  77. Dementia with Lewy Bodies: (DLB)
    • Histologically indistinguishable from Parkinson – Parkinsonian motor features (usually confused with PD)
    • Prominent visuospatial and executive deficits
    • Fluctuating cognitive impairment
    • Psychiatric disturbance; anxiety, VISUAL HALLUCINATIONS
    • ONSET MORE RAPID THAN PD (within 12 months of motor symptoms compared to PPD where dementia occurs 4-5 yrs after motor symptoms)
  78. Vascular Dementia:
    • Single or multiple infarcts
    • Mechanism – ischemia/thrombosis, or hemorrhage
    • Symptoms depend on location of infarct
    • STEPWISE OF PROGRESSIVE ACCUMULATION OF COGNIITIVE DEFICITS – dementia usually within 3 months of event
    • Common co-morbidities:
    • DM, HTN, CAD, PVD
  79. Alzheimer’s Disease (AD):
    • Most common age related (usually after 60) neurodegenerative dz. (risks doubles every 5 yrs)
    • Positive family history in 50% of cases
    • Progressive intellectual deterioration
    • Executive impairement
  80. Ad Pathology:
    • Senile plaques = extracellular deposits of beta-amyloid peptide surrounded by dystrophic axons
    • Neurofibrillary tangles = intracellular accumulation of phosphorylated tau protein
  81. AD Progressive intellectual deterioration
    • Short term memory impairment is early and prominent:
    • Repetitive speech in conversation
    • Difficulty remembering conversations, events, appointments
    • Misplaced objects
  82. AD Executive impairment:
    • Decline in complex task performance
    • Decline in problem solving ability
    • Impairment in driving
  83. AD Early Stages (0-4 yrs.)
    • mild decline in memory/executive function
    • +aphasia, apathy, depression
  84. AD Middle Stage (5-8yrs.)
    • moderate decline in memory/executive function
    • +poor insight, agitation, psychosis
  85. Ad Advanced Stages (9-12 yrs.)
    severe (ie. forget how to feed themselves)
  86. Alzheimer’s Disease Treatment:
    • Treat symptoms early:
    • Depression – SSRI (Paxil, Prozac, etc.)
    • Insomnia – Trazodone (Desyrel) 25 – 100 mg qhs
    • Moderate anxiety or restlessness – short acting benzodiazepine (Xanax, Ativan, etc.)
    • Severe aggressive agitation – risperidone (Risperdal) 0.25 – 1.0 mg bid
  87. AD Cholinesterase inhibitors
    • for memory enhancement and to slow disease - increases acetylcholine (can take 6 wks for full effectiveness)
    • Mild to Moderate symptoms: Donepezil (Aricept) 5-10 mg qd
    • Rivastigimine (Exelon) 3-6 mg bid (less GI side effects) (Patch)
    liver dz., PUD, severe COPD, bradycardia/SSS
  89. Glutamate receptor antagonist ad
    • moderate to severe disease – decreases activation of NMDA receptors (N-methyl-D-aspartate) (can take months to see memory improvement/arrest progression)
    • Memantine (Namenda) 5-10 mg bid
  90. Cluster HA
    • severe, unilateral, localized in periorbital area and temple
    • At least one of these: Ipsilateral lacrimation, nasal congestion, miosis/ptosis, eyelid/facial edema, restlessness/agitation
    • More common in men (>30 yo) (occur at later age in women)
    • Attacks can last 1 hr – 3 hrs and can occur 1 -6 times a day (commonly wakes people from sleep)
  91. CLUSTER Episodic
    : attack phase lasting 1-4 months followed by cluster free period of 6 months to years duration
  92. Cluster Chronic
    with a cluster free interval of <1 week in a 12 month period of time
  93. cluster Treatment:
    • Oxygen 100% at 7-10 liters for 10-15 mins
    • Sumatriptan (Imitrex) 6mg SC (max. of 12mg in 24 hrs. with at least 1 hr in between injections)
    • (Contraindicated in CAD)
    • Dihydroergotamine (DHE) (IV, SC, IM, nasal spray)
  94. Cluster Prophylactic Tx
    verapamil, Topiramate (Topamax), Divalproex (Topamax)
  95. Migraine HA:
    • Episodes vary - can last 4-72 hrs., frequency can be from once weekly to less that one per year
    • Childhood = Male>Female
    • Female>Male after menarche to mid-adult life
  96. Migraine Risk factors:
    • Specific foods (aged cheese, red wine)
    • Medications
    • Family history (>80%)
  97. Migraine dx requires 2 of:
    • 1.Unilateral
    • 2.Pulsating
    • 3.Moderately severe.
    • 4.Aggravated by physical activity
  98. Migraines phases
    • 5
    • Prodrome / Aura / (Early) HA / (Late) Resolution / Postdrome
    • Without aura (common migraine) 80%
    • With aura (classic migraine) – disturbance of neurological function prior to headache onset
  99. Phase I: Prodrome
    drowsiness, talkativeness, hunger, depression, yawning, irritability, tension, nausea
  100. Phase II: Aura
    • onset over a 5-20 min, last <1hr., visual MC: twinkling, geometric, hemianopsia
    • Phase III: HA
    • 60% one side, 40% bilateral, throbbing, N/V, aversion to light/sound, mvt. worse
  101. Phase IV: Resolution
    pain improved, few symptoms remain; impaired concentration, fatigue nausea
  102. Phase V: Postdrome
    “migraine hangover” fatigue, scalp tenderness
  103. Migraine Abortive Tx.:
    • Triptans: 5-HT-1 agnoists (during early/mild phase)
    • Sumatriptan (Imitrex) SC 4-6 mg once, repeat once after 2 hrs if needed (max 12 mg in 24hrs.)
    • Contraindicated in CAD, PVD, uncontrolled HTN
    • Ergotamine tartate and caffeine (Cafergot) 1/100 mg (1-2 at start of HA the 1 every 30 mins as needed, max if 6 mg/day)
    • Contraindicated in CAD, CVD
  104. Migraine Prophylactic Tx:
    Topiramate, Valporic acid, Beta Blockers, Amitriptyline
  105. Tension HA
    bilateral, in frontal-occipital lobes or generalized, band-like pressure, muscular tightness or stiffness in neck
  106. tension Two types:
    • Episodic – associated with stressful event
    • Chronic – often recurring daily associated with contraction of muscles back of neck and scalp
  107. Tension Causes:
    poor posture, anxiety, depression, TMJ syndrome, dental dz, HTN, OA of cervical spine
  108. tension ha Treatment:
    • NSAIDs (motrin, advil) 400mg tid
    • Naproxen sodium 500 mg bid
  109. Tension ha Prophylactic Tx
    : SSRI’s, TCA
  110. Parkinson’s Disease: neurodegenerative disorder of extrapyramidal motor system, imbalance between dopamine and acetylcholine, occurs in Male>Female, onset ~60 yo.
    Loss of pigmented cells in substantia nigra that make and store dopamine
  111. Parkinson Cardinal Signs
    Tremor at rest, rigidity, bradykinesia, postural instability
  112. Parkinsons ssx Other
    poor enunciation of words, ocular abnormalities, depression (75%), dementia, sleep problems
  113. PARK Stage 1:
    unilateral minimal functional impairment (infrequent blinking)
  114. PARK Stage 2
    bilateral without impairment of balance (lack of facial expression = “masked facies”)
  115. PD Stage 3
    bilateral, with instability and physically independent
  116. PARK Stage 4:
    Severe disability, can walk/stand without help but markedly incapacitated
  117. PD Stage 5
    heelchair or bedridden unless aided
  118. PDtx
    • GOAL: to get more dopamine to the brain
    • Surgery: deep Brain stimulator-if meds fail
    • Dopamine agonist
    • Levodopa/carbidopa
    • COMT inhibitor
    • Mao-B, anticholinergics
    • 2nd line: antiviral
  119. Dopamine Agonist ie Mirapex/rotigotine
    Parkinsons initial therapy, may delay need for levodopa
  120. Dopamine Agonist:
    Pramipexole (Mirapex), Ropinirole (Requip), Patch Rotigotine (Neupro)
  121. Levodopa/Carbidopa (Sinemet)
    • 40-50% improvement in motor function –
  122. Catechol-O-methyltransferase inhibitor (COMT inhibitor) (
    • taken with levodopa (blocks breakdown of levodopa)
    • PD med
  123. COMT inhibitor
  124. Monoamine oxidase-B inhibitor (MAO-B):
    • used in late stage,
    • blocks enzyme in brain that breaks down levodopa (boost effects of Sinemet)
  125. MAO-B
    Elderpryl/Carbex (Selegiline) –
  126. Second-line - Anticholinergics:
    Benzotropine (Cogentin), Trihexphenidyl (Artane):
  127. Second-line – Anticholinergics Benzotropine
    decrease acetylcholine which controls movement
  128. Antiviral Amantidine (Symmetral)
    reduced motor fluctuations, used in mild, early PD
  129. Essential Tremor or Familial Tremor
    • unknown cause
    • Advanced age is a risk factor, if genetically predisposed onset can be younger age
    • Emotional stress enhances symptoms
  130. Essential tremor ssx
    • involuntary, rhythmic, oscillatory movement
    • can present as resting tremor, action tremor, or intention tremor
    • spreads proximally, does not reduce life expectancy
    • Head tremor more common in women
  131. Essential tremor Treatment
    • Propranolol, Primidone,
    • clonazepam (Klonopin), carbamazepine (Tegretol)
    • Surgery: Thalamotomy – ablative
    • Deep Brain stimulator – non-ablative
  132. Myasthenia Gravis
    • autoimmune d/o = pure motor syndrome
    • blocked neuromuscular transmission at acetylcholine receptor
    • Occurs typically 20-40yr : females peak in 3rd decade, males peak in 5th-6th decade
  133. MG ssx
    • Muscular Weakness: onset mild, intermittent over years, worse in the evening
    • PTOSIS(25%)
    • DIPLOPIA 25% Dysphonia
    • PROXIMAL LIMB WEAKNESS; Facial weakness
    • Fatigue on chewing; Neck weakness
    • Dysarthria (10%); Dysphagia (10%)
  134. Mg dx
    • Tensilon Test (edrophonium):
    • Other test: EMG,
    • immunoprecipitation assey (80-90% show antibodies in serum)
  135. Tensilon test-MG
    Diagnostic – grip strength improves within 30 secs.
  136. Myasthenia Gravis Treatment:
    • Anticholinesterase therapy:
    • Surgical: Surgical: Thymectomy (not for very old or very young)
  137. Anticholinesterase therapy MG
    • Mestinon (Pyridostigmine bromide)
    • Prostigmin (Neostigmine)
  138. Immunosuppressant therapy MG
    • Prednisone
    • Azathioprine (Imuran)
    • Cyclophosphamide (Cytoxan)
    • Plasmaphoresis
    • IVIG
  139. Guillain-Barre Syndrome
    • autoimmune d/o, demyelination of peripheral nerves
    • Early signs paresthesias of hands and feet
    • Usually in ASCENDING WEAKNESS/PARALYSIS OF LIMBS (moves distal to central)
    • Gait affected, back and leg pain common, RESPIRATORY MUSCLE PARALYSIS (30% if untreated)
  140. Gb Follows
    50-70% of cases follow infection (Campylobacter jejuni enteritis), viral URI or surgery
  141. Gb Diagnostics:
    • Creatinine Kinase elevated (2-5 fold), LP (CSF)=elevated proteins, normal WBC
    • Electrophysiology – marked slowing of conduction
  142. Gb Treatment:
    • IVIG, Plasmaphoresis,
    • symptomatic/supportive treatmen
    • hospitalize for cardiopulmonary support (when needed)
  143. Bell’s Palsy
    unilateral paralysis/weakness of facial muscles (supplied by CN7)
  144. bellsy palsy Associated with
    • Herpes zoster, Lyme dz.,
    • sarcoidosis, Guillian-Barre, MS, DN, cancer, trauma,
    • viral infection
    • Most common over age 30
  145. Bells palsy Signs/Symptoms:
    • acute onset, unilateral total or partial paralysis of face muscles,
    • numbness, ptosis, decreased nasolabial fold
    • Ipsilateral; loss of taste,
    • ear ache, inadequate tear production, loss of corneal reflex
  146. bells palsy Treatment
    • most resolve spontaneously (10% may have permanent disfigurement)
    • Oral corticosteroids or prednisone, (eye patch)
    • Start tx immediately for better outcomes
    • (if patient presents with complete paralysis – less likely to have full recovery
    • if complete paralysis at day 5 refer to neurologist
  147. Diabetic Peripheral Neuropathy
    • Diabetes is the most common cause
    • can affect any peripheral nerve
    • Associated with hyperglycemia, nerve infarct, vascular insufficiency
  148. DPN Signs/Symptoms:
    • “Stocking/glove” presentation:
    • common in toes/distal feet (later in hands)
    • Tingling, burning,
    • abnormal pain and temp. sensation,
    • reduced vibratory sensation, Achilles reflex
  149. DPN Diagnosis
    nerve conduction studies
  150. dpn labs r/o other causes
    • uremia, EtOH, vasculitis
    • B12 deficiency, hypothyroidism, amyloidosis
  151. DPN Treatment
    • tight control of serum glucose! Multiple agents are used for management
    • Tricyclic antidepressants – amitriptyline, nortriptyline
    • Anticonvulsants – carbamazepine (Tegretol), Gabapentin (Neurontin)
    • Pain management – lidocaine patch, tramadol (Ultram)
  152. Multiple Sclerosis
    • inflammatory process, multifocal demyelinization of the white matter in brain and spinal cord, unknown cause; autoimmune theory triggered by genetic susceptibility vs viral (EBV)
    • More common in women – 16 to 40 years of age, caucasian/European decent
    • Course – New neurologic symptoms in young person intermittent, progressive
  153. MS Signs/Symptoms:
    • Multiple and varied neurologic signs/symptoms
    • Ataxia +Babinski sign Clumsiness
    • Fatigue Hand paralysis (tingling) Blurred vision in one eye (retrobulbar neuritis)
    • Loss of position and vibration sense Clonus
    • Sphincter disturbance urinary urgency/hesitancy
  154. Ms Clinically Isolated Syndrome
    (initial episode): weakness, numbness, tingling, unsteadiness
  155. MS Relapsing-Remitting Disease
    • an interval of months to years after initial episode before new or recurring symptoms (acute relapses) followed by recovery (resolution of inflammation, myelin repair)
    • Exacerbations may be triggered by infection, pregnancy
  156. Ms exacerbations triggered by
    Infection and pregnancy
  157. MS Secondary Progressive Disease
    • relapses with incomplete remission, does not return to baseline, steady deterioration
    • Optic atrophy, nystagmus, dysarthria, pyramidal, sensory, cerebellar deficits
  158. MS Primary Progressive Disease
    • (less common) symptoms are steadily progressive from the onset
    • Disability occurs at early stage
  159. Multiple Sclerosis Diagnostic Studies
    • MRI (more sensitive than CT) – shows many plaques – DAWSON’S FINGERS
    • Visual evoked response (VER) – abnormal in 75-97% of MS cases
    • CSF: elevated protein (especially after acute relapse) (myelin basic protein from destruction)
    • Elevated IgG and discrete bands of IgG (oligoclonal bands)
    • Glucose usually normal
    • *Clinically definite disease is made in patients with relapsing/remitting MS and at least
    • 2 lesions involving different areas of the CNS white matter
  160. Multiple Sclerosis SYMPTOMATC TX
    • Corticosteroids - Methyprednisolone - for acute attacks
    • IVIG may control relapses
  161. MS Disease Modifying Treatment (DMT)
    • reduces frequency of relapses, may delay disability
    • Interferon-B 1a (Avonex, Rebif, Betaseron) or Interferon –B 1b (Betaseron/Extavia)
    • Natalizumab (Tysabri®) - immunomodulator
    • Fingolimod (Gilenya®)
    • Novantrone (Mitoxantrone) - immunosuppressant
  162. MS Supportive:
    • Spasticity – Bacolfen
    • Neuropathic pain – gabapentin
    • Chronic fatigue - amantadine
  163. Seizures
    • transient disturbance of cerebral function due to abnormal paroxysmal neuronal discharge in the brain
    • increase risk of sudden death by 5-11 fold
  164. Serial seizures
    seizure then consciousness the seizure again
  165. Status epilepticus
    further convulsions without consciousness between attacks
  166. SEIZURES Causes
    • idiopathic (no cause no neurological abnormality)
    • Pediactric age group – congenital abnormalities or prenatal injury
  167. seizures Secondary causes
    • febrile,
    • metabolic (EtOH, drugs, uremia, hypoglycemia),
    • trauma, neoplasm,
    • vascular (infarct, ischemia, AVM’s),
    • infectious (reversible, meningitis/encephalitis)
  168. Seizures Classifications:
    • PARTIAL: simple & complex
    • Generalized: absence, tonic-clonic
  169. Partial Seizures = Focal Seizure
    affects only part of the brain
  170. Simple Partial Seizure
    • no LOC, isolated tonic OR clonic activity,
    • transient altered sensory perception, ]’
    • march/spread down extremity (Jacksonian March),
    • light flashes, buzzes, déjà vu, illusions
  171. Complex Partial Seizure
    • no LOC, characterized by aura, N/V,
    • will not remember all or part of seizure,
    • focal tonic or clonic activity, automatism (lip smacking, chewing, stroking, rubbing hands), last 1-3 mins, often confused after, it takes 5-10 mins to come around
  172. Generalized Seizures =
    affects entire brain
  173. Absence (Petit Mal)
    • Generalized seizure
    • misses words in conversation,
    • brief impairment (<20 sec) patient usually unaware,
    • impaired consciousness “blank stare”,
    • mild tonic or clonic or atonic components,
    • starts in childhood stops by age 20, but can progress to other types of seizures
  174. Tonic-clonic (Grand Mal):
    • this is what we think of as epilepsy
    • tonic phase - lasts <1min. = sudden LOC, falls to floor, may “cry out”, may bite tongue
    • clonic phase – jerking or convulsing, grunting, pale/cyanotic lasts 2-3 mins., then flaccid coma consciousness sleep postictal period
  175. Postictal phase
    HA, confusion, drowsiness, nausea, muscle soreness - lasts mins. to hours
  176. Tonic seizure
    : all muscles go stiff, patient becomes rigid then falls, very short period, recovers quickly
  177. Atonic seizure:
    all muscles go limp/floppy, patient falls usually forward, “drop attach”, recovers quickly
  178. Myoclonic seizure:
    muscle jerk, arms and legs briefly jerk (like when we fall asleep)
  179. SeizuresDiagnostic Studies:
    • Imaging MRI (more sensitive than CT), order if new onset seizure, if focal neurologic signs/symptoms, if EEG shows focal disturbance, if progression of symptoms
    • CBC, CMP, Calcium, Magnesium, CSF(if acute setting, new onset seizure)
    • EEG – standard or 24 hr -72 hr ambulatory monitoring
  180. Treatment: goal is to control seizures using one medication (65% will need one, 35% need two) and to reduce drug interactions (especially with warfarin, CCB)
    • Antiepileptic Drugs (AED’s) = First Generation : Phenytoin (Dilantin), Carbamazepine (Tegretol), Valproate/Valproic acid (Depakote), Phenobarbital (Luminal)
    • Second Generation: Levatiracetam (Keppra), Gabapentin (Neurontin), Lamotrigine (Lamictal), Topiramate (Topamax), Pregabalin (Lyrica)
  181. Status Epilepticus
    • epileptic seizure that last >30 mins. or absence of full recovery of consciousness between seizures, cardiac and respiratory changes, cerebrovascular changes, postictal findings
    • Is life threatening, can cause permanent brain damage due to hyperthermia, circulatory collapse
  182. Status epilepticus Causes
    • : febrile convulsions,
    • acute or chronic CNS injury
    • , intoxication, idiopathic
  183. Status epilepticus Treatment:
    • rapid control of seizure is critical to survival – ABC’s
    • LORAZEPAM (Ativan) IV or Diazepam (Valium) IV and Phenytoin (Dilantin)
    • If persist after 5 mins. Add Fosphenytoin (Cerebyx)
    • If seizure persist/refractory status – ICU - induce drug coma Phenobarbital (Luminal) or Propofol (Diprivan)
    • Once seizure controlled – prophylactic therapy
  184. Normal CSF results in adults:
    • Appearance: Clear (normal)
    • Opening pressure: 10-20 cm H 2 O
    • White cell count: 0-5 cells/µL (< 2 polymorphonucleocytes [PMN]);
    • (normal cell counts do not rule out meningitis or any other pathology)
    • Glucose- CSF:Serum glucose ratio: 0.6 (>60% of serum glucose)
    • Protein level: < 45 mg/dL (0.45 g/L)
  185. CSF results for Bacterial meningitis:
    • Appearance: Clear, cloudy, or purulent (turbid)
    • Opening pressure: Elevated (>30 cm H 2 O)
    • WBC count: >100 cells/µL (>90% PMN); partially treated cases may have as low as 1 WBC/µL
    • Glucose – CSF:serum ratio: decreased 0.4 (< 40% of serum glucose)
    • Protein level: Elevated (>50 mg/dL)
    • Consider additional tests: CSF Gram stain and cultures, blood cultures, CSF bacterial antigens, CSF polymerase chain reaction (PCR), others depending on clinical findings
  186. CSF results in Aseptic (viral) meningitis:
    • Appearance: Clear
    • Opening pressure: Normal or mildly elevated
    • WBC count: 10-1000 cells/µL (lymphs but PMN early)
    • Glucose – CSF:serum ratio: >0.6 (>60% serum glucose, may be low in HSV infection)
    • Protein level: normal or slightly elevated (>50 mg/dL)
    • Consider additional tests: CSF Gram stain and cultures, blood cultures, CSF bacterial antigens, CSF PCR (eg, herpes simplex virus [HSV], varicella-zoster virus [VZV])
  187. CSF results in Fungal/TB infection:
    • Appearance: clear or opalescent (fibrin web)
    • Opening pressure: often elevated
    • WBC: 10-500 lymphocytes
    • Glucose – CSF:serum ratio: decreased <0.4 (20-40%)
    • Protein: increased but usually <500mg
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