Syndromes Mononeuropathy: Carpal tunnel syndrome Polyneuropathy: Diabetic, Alcoholic Post-herpetic neuralgia Neuropathic Pain Syndromes Complex Regional Pain Syndrome Type I (Reflex
Sympathetic Dystrophy) Initial noxious event involving distal extremity, pain disproportionate to injury, not limited to single nerve distribution. Associated with edema, changes in skin blood flow. Neuropathic Pain Syndromes Complex Regional Pain Syndrome Type 2 (Causalgia) Sequela of injury to nerve or major branch (esp. median, sciatic,
tibial, and ulnar nerves). Thalamic Pain: DejerineRoussy Syndrome Due to thalamic infarct or other lesion. Hemi-anesthesia followed by gradual return of sensory function and pain. Pain contra-lateral to lesion. Headaches
Headaches Tension headache Dull, bilateral, band like, chronic in course and usually related to stress. Tx: NSAID, rule out Major Depression Migraine: at least five episodes of Episodic Headache lasting four to seventy two hours Any two of:
Unilateral Throbbing Worsened by movement Moderate or Severe Any one of: Nausea or vomiting Photophobia and
headache Ipsilateral lacrimation and nasal congestion with rhinorrhea Usually triggered by Treatment: 100% Oxygen (Air Supply) Cluster Headache
Rare Disorder (0.1-0.4% of population) Age of onset 20s-30s Clinical features: Excruciatingly severe, retro-orbital pain. Radiates to temple, teeth, neck. Last 15-180 minutes. Ipsilateral autonomic features, pacing, nocturnal attacks often awaken them. Triggers: Alcohol, Nitroglycerin. Cycles usually occur spring and fall and last 4-12 weeks. Cluster Headaches Acute
Brain Hemorrhages Subdural, Epidural and Subarachnoid Hemorrhages Subdural Hematoma Suspect in older patient with newonset headache Follows head trauma Tearing of bridging veins Extra-axial mass
causes focal findings Waxing and Waning mental status Concave on CT Epidural Hematoma Between bone and dura Associated skull fracture in 85% of
adults Middle meningeal artery tear Brief LOC, initial lucid period then acute deterioration Convex on CT Subarachnoid Hemorrhage Cause: Rupture of aneurysm or AV
malformation. Clinical feature: sudden onset of worst headache of my life Studies: CT scan. LP will show blood and Xanthochromia (yellow heme pigment) Tx: Clip aneurysm Athena and Zeus Subarachnoid Hemorrhage
Occipito-nuchal Sentinel bleeds Most common cause? Trauma Dementias Alzheimers Disease Extracellular deposition of amyloid-beta protein, intracellular neurofibrillary
tangles, and loss of neurons. CT: Atrophy, ventricular dilatation Treatment: CJD vs. AD CJD AD Course Six months (rapid) Insidious (years to decades)
Physical findings Myoclonus EEG Periodic complexes, burst-suppression CSF 14-3-3 protein (>90%), some false + Pathology Spongiform changes Plaques and tangles
Transmissibility Person to person and person to animal Non-transmissable Slowing of background Huey, Dewey and ..Lewy Body Dementia
Personality change Decline in function Poor social judgment Inappropriate Pathology: Prominent frontotemporal atrophy, neuron cell inclusions, clustered cytoskeletal elements NPH wouldnt do that! Triad: an imbalanced, wide-based walk or shuffle, urinary
incontinence and MEMORY PROBLEMS. Dementia predominantly frontal lobe in nature, with apathy, dullness in thinking, and slight inattention. Memory problems are usually main problem, which can lead to the misdiagnosis of AD. Neil Patrick Harris, aka Doogie Howser, MD Normal Pressure Hydrocephalus
Dementia Incontinence Gait apraxia (magnetic gait) Subacute Sclerosing Pancephalitis (SSPE) Dementia and myoclonus with onset in childhood
Course usually rapid and fatal, may be aborted with antiviral drugs CSF has anti-measles antibodies, and EEG shows periodic or burst-suppression Cause probably measles or measles-like virus Neuropathology power-review Parkinsons, Huntingtons, Duchennes, ALS, Guillian Barre, Myasthenia Gravis, Multiple Sclerosis, Seizure Disorder, and Brown-Sequard Syndrome. Parkinsons Disease Cardinal Features
Tremor: resting, pill-rolling, coarse, 3-5 Hz. Rigidity: cogwheel Bradykinesia or akinesia Minor Features Festinating gait: small accelerating steps with decreased arm swing. Postural reflex
abnormalities including a positive pull test Hypophonia, Micrographia Sleep Disturbances (partly iatrogenic from dopamine agonists) Huntingtons Disease Atrophy of cerebral cortex and head of caudate nuclei leads to compensatory enlargement of lateral ventricles (batwing). Excessive Cytosine-Adenine-Guanine (CAG) trinucleotide repeats (other illnesses with excessive trinucleotide repeats include: Myotonic dystrophy, Fragile X syndrome, many forms of
Spinocerebellar degeneration). Duchennes Type Muscular Dystrophy Sex-linked recessive inheritance with onset in early childhood Caused by loss of muscle membrane protein, dystrophin Pseudohypertophy (especially in calves) Proximal weakness: requires arms to arise from chair or floor
DTRs decreased except for Achilles reflexes (ankle) Elevated muscle enzymes: CPK, aldolase UMN vs. LMN Sign and Symptoms Upper Motor Neuron Lower Motor Neuron Reflexes Hyperactive Hypoactive Babinski sign
Present Amyotrophic Lateral Sclerosis Combines UMN and LMN symptoms Asymmetric limb weakness = most common presentation. Limb fatigability, twitching, wasting, and stiffness. Bulbar onset (2nd most common type)
features dysarthria and dysphagia. Lou Gehrigs disease Clinical Case Scenario A patient develops progressive weakness two weeks after a viral infection. What is possible diagnosis and what tests would you order? Acute Idiopathic Polyneuropathy Guillain Barre Syndrome Guillain-Barre
Symmetric weakness, usually beginning in the legs, and more marked proximally than distally. Some sensory complaints. Typical absence of deep tendon reflexes. May be marked autonomic dysfunction. Slow conduction velocity CSF shows increased protein concentration but normal cell count. Electrophysiology shows marked slowing of motor/sensory nerve conduction velocity (denervation and axonal loss) Guillain-Barre
Treatment: Plasmapheresis or IV IG Myasthenia Gravis Insidious onset. Slowly progressive course. Diplopia, dysarthria, ptosis, extremity and generalized weakness not conforming to distribution of any single nerve. Pupillary responses not affected. Persistent activity of a muscle group leads to temporary increase of weakness > restoration of strength after brief rest.
Myasthenia Gravis Edrophonium challenge test (screening) EMG Confirmatory: Ach receptor antibody test Tx: Neostigmine, Pyridostigmine (if poor response: Corticosteroid). Consider Thymectomy in all patients < 60 yr unless only extraocular weakness.
Multiple Sclerosis Relapsing remitting symptoms Separated in space and time MRI: Multiple periventricular plaques in white matter. Oligoclonal bands in CSF.
Internuclear ophthalmoplegia When the patient attempts to look to left, left eye turns with nystagmus (abducted eye) and right eye cannot turn to left (impaired adduction).
Location of lesion: Medial longitudinal fasciculus. Young adults: MS most common cause Older patients: vascular diseases. Seizure Disorder Partial Seizures: originate in a focal region of a single hemisphere Simple Partial Seizures: no alteration of consciousness Secondary Generalization: spreads to both hemispheres
Complex Partial Seizures: alteration of consciousness Brief Duration (i.e. 2-3 minutes); May have motionless staring or automatisms (involuntary motor behaviors) Generalized seizures: involve both cerebral hemispheres from the outset (4). brief loss of muscle tone or flexion) (1). Atonic Tonic: Seizure: sudden muscular rigidity (extension (5). ("petit mal") a few seconds (2) Absence
Brown-Sequard Syndrome Contra: loss of P and T, Ipsi: loss of vib./joint position, paralysis, hyperreflexia, Babinski CSF in Meningitis Diagnosis Cells Glucose (mg/dl) Protein (mg/dl) Opening
Pressure Normal 0-5 lymphocyt e 45-85 15-45 70-180 Aseptic,vir al 25-2000, mostly lymphocyt es
NORMAL High > 50 Slight elevation Bacterial 20020,000 Polymorph s, neutrophil s Low <45 High >50 Markedly
high Tuberculos is 100-1000 lymphocyt es Low <45 High > 50 Moderate Elevation LOCALIZATION OF STROKES The Circle of whatchu talkin bout Willis?
Anterior Cerebral Artery Profound lower extremity weakness (contralateral) Stroke may result in paralysis/sensory loss in contralateral leg and foot. Middle Cerebral Artery Profound upper
extremity weakness (contralateral). Contralateral hemiplegia, hemisensory loss and homonymous hemianopia, eyes deviated to side of lesion. Apraxia/neglect. If left lobe involved: Global aphasia. Posterior Cerebral Artery Contralateral homonymous
hemianopia, with macular sparing. Prosopagnosia (inability to recognize faces) Vertebrobasilar Artery Vertigo Nausea and
vomiting Drop Attack Vertical Nystagmus Dysarthria/ dystonia Ataxia Labile Blood Posterior inferior cerebellar artery Lateral Medullary or Wallenbergs syndrome
Sensory loss of the FACE 9 and 10 C.N. damage Limb ataxia Horners syndrome Spinothalamic sensory loss Pure Motor Stroke Weakness of face, arm, and leg on one side of body (without cognitive, sensory, visual abnormalities) favors presence of thrombotic stroke involving penetrating arteries or small intracranial hemorrhage.
(stroke or congenital abnormality). Associated with learning disabilities, rightsided paresis and hyperactive Category Non-fluent Aphasia Fluent Aphasia Previous terms (not synonymous) Expressive, Motor, Brocas, Anterior Receptive, Sensory,
Wenickes, Posterior Spontaneous Speech Output: Sparse < 50 WPM, single words Content: Nouns and Verbs primarily, Dysarthric, Telegraphic Output: Plentiful > 100 WPM, entire phrases, Paraphasias (incorrect words, clang associations, neologisms) Response to Tests Comprehension Preserved but Naming
and Repeating impaired Comprehension Impaired (variable) and Naming and Repeating impaired Associated Deficits R-sided hemiparesis (arm > leg) Minimal hemiparesis, hemianopia, hemisensory loss Etiology CVAs, trauma, other focal lesions
Focal lesions, sometimes frontotemporal dementia, AD, cerebral anoxia Location of Lesion Frontal lobe, especially L Temporal or parietal MCA lobe Variants of Fluent Aphasia Conduction Transcortical (Isolation) Abnormality Cannot repeat
Can only repeat (echolalia), other functions variable Nature of Injury Disconnects arcuate fasciculus Isolates language arc from remainder of cortex Etiology Focal lesions Anoxia, CO poisoning, occasionally AD
Location of lesion Posterior temporal lobe Area(s) surrounding peri-sylvian arc Any questions?
Thank you to Stan Grant, Megan Rippy, Sunny Jiang, and Andrew Mehring, Nicole Patterson, Alex McCluskey, and Leyla Riley for their guidance, support, and dedication. This project has been funded by the NSF-PIRE. Special thanks to Melbourne Water, Trinity College,...
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