Neurology Review - James Rustad

Neurology Review - James Rustad

NEUROLOGY REVIEW James K. Rustad, M.D. Copyright 2010. All Rights Reserved. Lecture Outline Neuroanatomy Review Neurotransmitters: Dopamine, Norepinephrine, Serotonin Pain: Peripheral Nerve Fibers, Opiate Receptor Subtypes and Neuropathic Pain Syndromes Headaches (Tension, Migraine, and

Cluster Headaches) Brain Hemorrhages (Subdural, Epidural and Subarachnoid Hemorrhages) Lecture Outline Dementias: Alzheimers, CJD, Lewy Body, Picks, NPH, SSPE Neuropathology power review: Parkinsons, Huntingtons, Duchennes, ALS, Guillian Barre, Myasthenia Gravis, Multiple Sclerosis, Seizure Disorder, and Brown-Sequard Syndrome. Stroke Lesion Localization

Aphasias Neuroanatomy Review Frontal Lobe: Remember stimulation drives eyes contralateral and destruction induces ipsilateral eye movement. Prefrontal Region - Frontal lobe anterior to motor strip contains executive and inhibitory centers. Parietal Lobe: Stereognosis, two-point discrimination, visual association area (perception of visual symbols). Angular Gyrus (Gerstmanns syndrome). Occipital lobe: Visual cortex. Temporal lobe: Wernickes area. Mesial surface is

origin of most partial complex seizures. Neuroanatomy Review (continued) Basal Ganglia = Caudate nucleus, Putamen, Globus Pallidus, Subthalamic Nucleus, Substantia Nigra. Striatum = caudate nucleus and putamen. Lenticular Nuclei = globus pallidus and putamen.

Nigrostriatal tract (substantia nigra to striatum). Dopamine Metabolism Steps Phenylalanin e Phenylalan ine Hydroxylas e Tyrosine Epinephrine Tyrosine Hydroxyla se

(ratelimiting) Phenylamine NMethyltransfe rase DOPA DOPA Decarboxyl ase Dopami ne Dopamin e Beta Hydroxyla se Norepinephri ne Serotonin Synthesis Tryptophan

Converted by: Tryptophan Hydroxylase 5-hydroxytryptophan Amino acid Decarboxylase Converted by: Serotonin Breaks down to 5-HIAA (5-Hydroxyindoleacetic acid) Pain

Peripheral Nerve Fibers, Opiate Receptor Subtypes and Neuropathic Pain Syndromes Peripheral Nerve Fibers Type C fibers A-delta fibers Size Small Large Myelin No

Yes Conduction Velocity Slow Fast Character Dull, aching Sharp, brief Example Pancreatic cancer Burn Opiate Receptor

Subtypes Receptor Action Mu Analgesia, respiratory depression, constipation, miosis (pupillary constriction), euphoria Kappa Analgesia, dysphoria, disorientation/depersonalization Delta analgesia Neuropathic Pain

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

phonophobia Five Phases of Migraine Attack Phase I: Prodrome Phase II: Aura Phase III: Headache Phase IV: Headache Resolution Phase V: Postdrome

Migraine Treatments Acute Non-specific: NSAIDS, Combination analgesics, Opioids, Antiemetics, Neuroleptics. Specific: Ergotamine, Dihydroergotamine, Triptans. Preventive

Anticonvulsants (Divalproex, topirimate) Tricyclics Beta-Blockers Calcium Channel Blockers Cluster Headache M/F 6:1 Unilateral stabbing

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

Oxygen 5-10 Liters Sumatriptan injection (FDA approved) Ergotamine Preventive Prednisone Verapamil Lithium (for chronic cluster headaches) Divalproex

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

2nd commonest cause of degenerative dementia Progressive cognitive impairment Spontaneous onset Parkinsons symptoms Extreme neuroleptic sensitivity, Sleep problems, V/H Picks disease

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

Positive (dorsiflexion) Negative Muscle atrophy Absent Present Muscle tone Spasticity Flaccidity Fasciculation Absent

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

Clonic: generalized rhythmic jerkingof ofstaring/blank muscles, no initial look/unresponsive tonic phase (6). or widespread: non-rhythmic rapid (3) Myoclonic: Generalizedlocalized tonic clonic (may feature epileptic cry, apnea/ jerking movements of muscles cyanosis). Ictal activity 1-2 min; Post-ictal: incontinence, flaccidity, gradually return to normal consciousness. Disoriented, headache, sore mouth (oral trauma, muscular ache)

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.

Gerstmanns Syndrome Finger agnosia Left-right disorientation Agraphia Acalculia Dominant parietal lobe angular gyrus lesion

(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?

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