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  1. 1. NEUROLOGIC INVESTIGATIONS CSF Analysis CSF (general info): • Produced by choroids plexus of ventricles, absorbed through villi of arachnoid granulations that project into the dural venous sinuses • Production rate=.5 mL/min, total volume=150 mL, entire volume replaced every 5 hrs Lumbar puncture: • CI: space occupying lesion causing mass effect, increased ICP (LP can cause cerebral or cerebellar herniation) • CT: should be performed prior to LP (except in cases of suspected meningitis) • Complication: low pressure HA is most common (tx: pt should lie flat, increase liquid intake and caffeine) • Technique: o Pt position: lateral recumbent, legs flexed up over abdomen, pillow b/w legs o Level: L3-4 vertebral interspace (@ level of anterior superior iliac spine); spinal cord ends at L1-2 o Needle: inserted w/ bevel facing up, directed slightly rostrally to coincide w/ downward angulation of spinous process Interpretation of CSF findings: • Normal CSF: clear, colorless fluid w/ glc content 2/3 that of blood, trace ptn, <5 cells present (lymphocytes), opening pressure of 60-150 mm water RBCs No xanthocromia Traumatic tap Xanthocromia (yellow SAH, hemorrhagic encephalitis discoloration of supernatant of spun CSF sample) WBCs Polymorphs Bacterial or early viral infection Lymphocytes Infection (viral, fungal, mycobacterial), demyelination (MS), CNS lymphoma Elevated ptn Infection, demyelination, tumor, age Low glc Bacterial or mycobacterial infection Oligoclonal bands Demyelination (MS), CNS infections (Lyme Disease), Noninfectious inflammatory processes (SLE) Positive EBV PCR Highly suggestive of CNS lymphoma in pts w/ AIDS or other immunosuppressed states CT Concept • Characterizes degree of x-ray attenuation by tissue. Attenuation is the removal (by absorption or scatter) of x-ray photons and is quantified on an arbitrary scale (Hounsfield units) that is represented in shades of gray. Attenuation is dependent on atomic number and physical density of tissue. • Axial or coronal plane • Iodine is contrast agent used (if pt has allergy, do MRI instead); contrast enhancement indicates local disruption of blood-brain barrier Utility • Initial investigation used in variety of neuro d/o (HA, trauma, seizures, SAH, stroke) • Investigation of choice for demonstrating fresh blood Safety, tolerability, complications • CI: pregnancy MRI Concept • Uses radio frequency pulses (not x-rays). Images result from varying intensity of radio wave signals emanating from tissue in which hydrogen ions have been excited by a radio frequency pulse • Pt is placed in a magnet and then a radio frequency (RF) is administered o TE=time to echo, the time interval at which the signal intensity is measured o TR=time to repetition, the time between RF pulses • Gadolinium is contrast agent used Types • T1-weighted o Short TE/TR o Fat is bright, water (CSF) is dark
  2. 2. o Used to obtain gadolinium-enhanced images • T2-weighted o Longer TE/TR o Water (CSF) is bright • FLAIR (fluid attenuated inversion recovery) o Strong T2-weighted image, but one in which the signal from CSF has been inverted and is thus of low rather than high intensity o Used for demonstrating early or subtle T2 signal changes such as accumulation of edema • Susceptibility-weighted imaging o Sensitive to the distruptive effect of a substance on the local magnetic field (calcium, bone, blood b/d products ferritin and hemosiderin); areas of increased susceptibility appear black • Diffusion-weighted imaging (DWI) o Demonstrates cellular toxicity w/ high sensitivity o Most commonly used in diagnosis of acute stroke o Areas or restricted diffusion appear bright on DWI Utility • Provides better anatomic definition • Imaging of posterior fossa and craniocervical junction • DWI is most sensitive for demonstrating early tissue ischemia and is useful in evaluation of pts w/ suspected stroke Safety, tolerability, complications • Modality of choice in pregnancy • When contrasted imaging is required, MRI may be preferable to CT when there is a history of allergy to IV contrast (gadolinium and iodine are not cross-reactive), or liver disease (gadolinium is not nephrotoxic) • CI: metal objects, pacemaker/defibrillator devices, claustrophobia EEG Frequency patterns • Alpha (8-13 Hz): posterior head regions in relaxed awake state w/ eyes closed • Beta (14-30 Hz): frontal regions in relaxed awake state w/ eyes closed • Theta (4-7 Hz): drowsiness/sleep • Delta (.5-3 Hz): drowsiness/sleep Technique • Montage=pattern w/ which electrodes are connected to each other o Bipolar: all electrodes are active, records difference in electrical activity b/w 2 adjacent electrodes o Referential: electrical activity recorded beneath the active electrode relative to a distant or common average electrode Clinical utility • Limitations o Abnormal EEGs rarely are etiology-specific o EEG records electrical activity of cortical neurons, and thus surface EEG may be insensitive to dysfunction of deep structures o Interictal EEG may only be abnormal in 30% of adults w/ epilepsy • Abnormal patterns o Focal arrhythmic or polymorphic slow activity in theta/delta range local pathology in underlying brain o Generalized arrhythmic slow activity diffuse encephalopathy o Sharp and spike wave discharges w/ or w/o accompanying slow wave interictal epileptiform findings o Rhythmic spike or sharp and slow wave discharges or rhythmic slow waves focal or generalized electrographic seizures Nerve Conduction Studies (NCS) • Electrical stimulus applied over a nerve, and recordings are made from surface skin electrodes o Motor study: recording electrodes placed over end plate of a muscle innervated by nerve being stimulated; nerve stimulated in at least 2 locations (distal, proximal) and distance b/w 2 sites is measured  Distal latency=time interval b/w stimulation over distal portion of nerve and initiation of CMAP  CMAP=compound muscle action potential  Conduction velocity=calculated by measuring the difference in latency to CMAP initiation b/w proximal and distal sites of stimualtion
  3. 3. o Sensory study: nerve stimulated at one site; SNAP (sensory nerve AP) recorded either at more proximal site (orthograde study) or more distal site (antergrade study) • Utility: assists localization of pathology w/in PNS Nerve Conduction Studies in Demyelinating and Axonal Neuropathies Demyelinating Axonal Distal latency Prolonged Normal Conduction velocity Markedly reduced Normal; maybe slightly reduced CMAP amplitude Normal or mildly reduced Reduced EMG • Needle is inserted into individual muscles; recordings are made of muscle electrical activity upon insertion (insertional activity), while muscle is at rest (spontaneous activity) and during contraction (volitional motor unit potentials) • Utility: assists localization of pathology w/in PNS EMG in Neurogenic and Myopathic Disorders Neurogenic Myopathic Insertional activity Increased (active denervation) Usually normal Increased (necrotizing myopathies) Spontaneous activity Increased (active denervation) Usually normal Increased (necrotizing myopathies) Volitional motor unit potentials Large amplitude, polyphasic Small amplitude, polyphasic Recruitment Reduced Usually normal THE APPROACH TO COMA AND ALTERED CONSCIOUSNESS General • Coma=state of unarousable unresponsiveness • Describe alterations of consciousness in terms of a pt’s responses to various degrees of stimulation • Glasgow Coma Scale—has prognostic value in head trauma pts, is reproducible, and easy to use Clinical Approach to Altered Consciousness 1. ABCs: airway, breathing, circulation 2. Look for obvious clues to etiology a. Medical problems (diabetes, hepatic failure, seizure disorder) b. Circumstances in which patient was found c. Check for meningeal signs 3. Try reversing common reversible etiologies a. Naloxone (opiate OD) b. Thiamine (EtOH)—give before dextrose, which can precipitate Wernicke’s encephalopathy c. Dextrose 4. Check brainstem reflexes and look for focal signs a. Focal signs present suspect structural cause neuroimaging b. Focal signs absent suspect diffuse cause metabolic, toxic and/or infectious workup, neuroimaging Examination 1. Mental status testing a. Assess level of consciousness—an increasing gradient of stimulation should be applied and patient’s responses recorded b. For many pt’s, further cognitive testing may be impossible 2. Cranial nerve testing to assess brainstem function. Test these bs reflexes: a. Pupillary—II (afferent) III (efferent) b. Oculocephalic (doll’s eyes)—VIII (afferent) III, IV, VI (efferent)—forcibly turn head horizontally and vertically and observe for conjugate eye movement in opposite direction (CI if cervical spine injury not r/o) c. Caloric testing (if necessary, i.e., if turning head is CI or does not result in eye movement; never assume eyes are immobile unless caloric testing has been done)—inject 50 mL ice water into each ear and observe for conjugate eye deviation toward the ear injected d. Corneal—V (afferent) VII (efferent) e. Gag—IX (afferent) X/XI (efferent)
  4. 4. 3. Motor tone a. Motor tone b. Decorticate posturing—bs dysfunction slightly more superior that that of decerebrate posturing c. Decerebrate posturing—bs dysfunction 4. Muscle stretch reflexes, Babinski sign 5. Sensory testing usually limited to testing of light touch or pain sensation; applying nailbed pressure to each limb may be useful in looking for gross sensory abnormalities Differential Diagnosis General: • 2 ways in theory in which consciousness can be depressed: dysfunctional bs (e.g. pontine hemorrhage) or bilateral cerebral hemisphere dysfunction (e.g. hypoglycemia); BUT, unilateral cerebral hemisphere lesions, if large or severe enough to cause swelling and compression of opposite hemisphere or downward pressure on bs, can also lead to coma • General approach o +/- bs reflexes indicates how deep coma is o +/- focal signs narrows differential and guides workup  Structural causes of depressed consciousness: acute ischemic stroke, acute intracranial hemorrhage, brain tumor (w/ edema or hemorrhage), brain abscess  Diffuse causes of depressed consciousness: metabolic, toxic, infectious, hypoxic-ischemic (respiratory failure, cardiac arrest) Laboratory and Radiographic Studies • If STRUCTURAL cause is suspectedurgent head imaging, usually w/ noncontrast head CT; use CT rather than MRI even if focal brainstem signs are found (d/t possibility of a large cerebral hemisphere lesion compressing the bs) • If DIFFUSE cause suspected extensive metabolic, toxic, or infectious workup o Blood testing: CBC, electrolytes, glc, liver function tests o If infection suspected: chest x-ray, urinalysis, blood or urine culture, LP (BUT perform CT 1st! to avoid precipitating brain herniation) o Head imaging usually needed b/c it may demonstrate signs of global hypoxic-ischemic injury, diffuse cerebral edema, or bilateral lesions mimicking a diffuse process • EEG nonspecific, but can be of use in helping to assess how deep a coma is, based on degree of background slowing Treatment and Prognosis Treatment • Diffuse metabolic, infectious, toxic medical management • Structural neurosurgical intervention • If ICP increased raise head of bed, hyperventilation, osmotic diuretics (mannitol), corticosteroids for edema a/w brain tumors Prognosis • Depends on o Etiology o Age Special Topics 1. Persistent vegetative state—may follow prolonged coma and is characterized by preserved sleep-wake cycles and maintenance of autonomic functions w/ absence of awareness and cognition 2. Locked-in syndrome—awareness and cognitive function are preserved but almost complete paralysis occurs; cause by large lesions in base of pons 3. Brain death—irreversible cessation of all functions of the entire brain, including the brainstem a. Comatose b. Absent bs reflexes c. No spontaneous respirations even when PCO2 has been allowed to rise (apnea test) NEURO-OPHTHALMOLOGY
  5. 5. Anatomy • Coherent visual image: retinal axons lateral geniculate nucleus optic radiations in cerebral cortex primary visual cortex (visual area 1, Brodmann’s area 17, striate cortex). V1 receives visual info from contralateral visual hemifield. • Perception of motion, depth, color, location, form: V1 o Associative visual cortex (areas 18, 29) o Higher-order centers in posterior parietal and inferior temporal cortices Visual Loss +/- visual phenomena 1. Positive: brightness, shimmering, sparkling, hallucinations, shining, flickering, colors (suggest migraines or seizures) 2. Negative: blackness, grayness, dim vision, shade-obscuring vision (suggests stroke, TIA) Clinical evaluation of visual loss 1. Visual acuity problem in refractive apparatus of eye or optic nerve a. Hand-held Snellen b. Pinhole (if VA is poor) if pinhole test improves VA, then problem is in refraction c. If pt cannot read the letters count fingers perception of movement perception of bright light 2. Assessment of color vision a. Ishihara plates (red desaturation seen early in optic nerve problems [esp. optic neuritis]) 3. Test for afferent pupillary defects a. Size of pupil (anisocoria?) b. Light reaction, direct and consensual c. Accomodation (near reaction) 4. Visual fields 5. Ophthalmoscopic exam retinal nerve fiber layer damage, optic atrophy, swollen disc, abnormal disc, vascular lesions, retinal emboli Monocular visual loss v. binocular visual loss • Monocular suggests problems in eye, optic nerve, or chiasm • Binocular suggest chiasm or retrochiasmal lesion Visual Loss According to Localization Lesion Level Visual Field Defect Optic nerve Ipsilateral blindness Chiasm Bitemporal visual field defect (tunnel vision) Optic tract Contralateral homonymous hemianopia Optic radiations (parietal) Contralateral inferior homonymous quadrantonopia Optic radiations (temporal, or Meyer’s loop) Contralateral superior homonymous quadrantonopia Optic radiations (both) Contralateral homonymous hemianopia Occipital cortex Contralateral homonymous hemianopia w/ macular sparing Disorders of the Pupil Anatomy • Light retinal ganglion cells optic nerve optic chiasm optic tract pretectal midbrain nuclei (Edinger- Westphal) in rostral portion of 3rd nerve • Efferent PNS fibers from EW travel w/ CNIII (thru cavernous sinus), ultimately synapsing in ciliar ganglion sphincter pupillae (constrictor) • SNS innervates dilator pupillae o 1st order neuron: ipsilateral posterolateral hypothalamus down brainstem to IML @ C8-T1 spinal level o 2nd order neuron: synapse in superior cervical ganglion o 3rd order neuron: travel along internal carotid into cavernous sinus orbit Clinical Assessment Condition Signs/Symptoms Etiology Test Physiologic Asymmetric pupils Up to 25% of normal people Amount of anisocoria does not change anisocoria with different illumination Horner’s Ipsilateral miosis, ptosis, Impaired SNS innervation of pupil Cocaine eyedrops that fail to dilate the
  6. 6. syndrome ipsilateral anhidrosis abnormal pupil (neg) Hydroxyamphetamine eyedrops allows for pharmacologic localization if cocaine test is neg pre- v. post- ganglionic Horner’s (the pupil w/ post-gang Horner’s fails to dilate) CNIII palsy Mydriasis, ptosis, Compression of CNIII: initially (complete) ophthalmoplegia produces dilated pupil w/o compromising eye movements (b/c PNS fibers run in outer part of CNIII, while motor fibers are more internal) Vascular compromise CNIII ischemia (diabetes): normal, reactive pupil, but palsy of ocular muscles innervated by CNIII Adie’s pupil Dilated, with segmental Interruption of PNS supply arising LND: normally pupil constriction to (tonic pupil) contraction and light-near from ciliary ganglion light greater than to near stimulus; dissociation; anisocoria, opposite is true in LND (present when photophobia, blurred near there is a defect in light response as in vision optic neuropathy or d/t aberrant regeneration as in tonic pupil) Argyll Small, poorly reactive to Syphilis Robertson light but have preserved pupils near response (accommodation normal) Abnormal Optic Disc See pages 38-39 (table) Note: painful vision loss=optic neuritis; sudden painless vision loss=ischemia Diplopia Some Terms Used to Describe Eye Misalignment Strabismus Misalignment of eyes Comitant strabismus Misalignment is constant in all directions of gaze, and each eye has full ROM (ophthalmologic problem) Noncomitant strabismus Degree of misalignment varies w/ direction of gaze (neurologic problem) Phoria Misalignment of eyes when binocular vision is absent Tropia Misalignment of eyes when both eyes are opened and binocular vision is possible Anatomy of Eye Movements (SO4 LR6 AR3) • CNIII: dysfunction produces droopy dilated down and out; most common cause of CNIII dysfunction in older adults include microvascular occlusion and ischemia d/t HTN, diabetes mellitus and atherosclerosis; patterns of dysfunction include o CNIII nucleus: bilateral ptosis, weakness of contralateral superior rectus o Subarachnoid space: meningismus, constitutional sxs, CN defects o Tentorial edge compression: depressed level of consciousness, hemiparesis, hx of trauma or supratentorial mass lesion • CNIV: superior oblique intorts, depresses, adducts; dysfunction is worse on downgaze and pts c/o diplopia while reading and descending stairs and compensate w/ a contralateral head tilt (diplopia improves w/ head tilt away from side of lesion • CNVI: lateral rectus; o Lesions produce esotropia o Destruction of abducens nucleus in brainstem ipsilateral conjugate gaze palsy b/c of damage of interneurons connected to contralateral 3rd nerve through the MLF (medial longitudinal fasciculus) Clinical Evaluation of Diplopia • Ask: o Monocular or binocular? o If binocular, is it horizontal or vertical?
  7. 7. o Is it worse near or far? o Is the problem localized to an extraocular muscle (paresis or fatigue), brainstem MLF (internuclear opthalmoplegia), or to the orbit itself? • Tests o Cover test: detects a tropia; pt fixates on a small target, then cover one eye; watch other eye; if eye makes a refixation movement, this means that this eye was not aligned on the target; if eye moves nasally, pt has an exotropia, and if temporally, and esotropia; e.g. CNIII palsy exotropia and hypotropia of paretic eye; CNVI palsy produces esotropia of affected eye o Alternate cover test: detects phoria (eso or exophoria); phoria do not cause diplopia b/c eyes are aligned when both are opened simultaneously o Park’s 3-step test: detects CNIV palsy; 1) hypertropia of paretic eye 2) which increases when the pt looks to the opposite side and when 3) pt tilts the head to the same sider o Oculocephalic maneuver (doll’s eye test) o Saccades: rapid conjugate movement of the eyes between objects (fingertips); in general d/o of eye movements will produce slowness of saccades in the direction of the paretic muscle o Pupillary size and reflexes o Periocular signs or proptosis Horizontal Gaze • Internuclear opthlamoplegia (INO) o MLF connects CNVI nucleus w/ contralateral CNIII nucleus o Clinical characteristics of a RINO  Inability to adduct R eye in left lateral gaze  Nystagmus of abducting left eye  Adduction during convergence is maintained b/c this action does not depend on the MLF o Bilateral INOs can be seen in Wernicke’s encephalopathy • “One and a half syndrome” o D/t lesion of ipsilateral MLF + ipsilateral PPRF (paramedian pontine reticular formation=premotor substrate for ipislateral horizontal gaze) OR CNVI nucleus; causes are MS and brainstem ischemia o Clinical characteristics  Ipsilateral lateral gaze palsy and INO in contralateral lateral gaze  The only movement present in the lateral plane is abduction of contralateral eye Vertical Gaze • Controlled by rostral interstitial nucleus of the MLF (riMLF) located in the pretectal area near CNIII nucleus. Fibers controlling upgaze from riMLF cross to contralateral side using posterior commisure to communicate w/ inferior oblique and superior rectus subnuclei of CNIII complex • Abnormal vertical gaze movements d/t dorsal midbrain syndromes o Parinaud’s syndrome: upgaze disturbance, convergence-retraction nystagmus on attempted upgaze, light- near dissociation of pupils (d/t pineal tumor compressing dorsal midbrain) o Skew deviation: vertical tropia d/t brainstem or cerebellar lesion; hypotropic (lower) eye often on side of lesion Supranuclear Eye Movements Saccades: rapid eye movements that redirect the fovea to a new target • Voluntary horizontal saccades originate in frontal eye field and superior colliculus contralateral to the direction of gaze; these areas have direct connection to contralateral PPRF • Vertical saccades may also originate in frontal eye fields or superior colliculus but connect to contralateral riMLF • Ocular motor apraxia=inability to produce saccades • Abnormal saccades: hypermetric (overshoot), hypometric (undershoot); see table 4-6 on p. 42 Pursuit Movements: permit eyes to conjugately track a moving visual target to keep it in focus • Control is hemispheric and ipsilateral Vestibulo-ocular Reflex (VOR): coordinates eye movements w/ head movement, allowing visual image to not slip during head movement • Semicircular canals (rotation) and otoliths (linear acceleration)vestibular nucleiabducens nuclei CN III/IV via MLF • Abnormalities of VOR result in nystagmus:
  8. 8. Nystagmus: rhythmic to-and-fro movement of the eyes • Types o Rhythmic o Jerk: eye drifts away from fixation in a pursuit-like movement and returns with a fast, saccadic movement; the direction of nystagmus is named by the direction of the saccadic fast component • Etiologies o Congenital o Physiologic o CNS dysfunction, peripheral vestibular loss, visual loss  Peripheral: usually unidirectional, w/ fast phase away from the side of the lesion; combines horizontal and torsional movements and is inhibited by fixation; tinnitus or deafness often present; severe vertigo; duration is short by recurrent  Central: normally bi-directional, often purely horizontal, vertical, or torsional, and not inhibited by fixation; tinnitus and deafness rarely present; mild vertigo; duration may be chronic • See table on p. 43 (4-7) THE APPROACH TO WEAKNESS Approach to Weakness Flowchart 1. Make sure that true weakness (i.e. decreased strength) is the complaint (NOT general sense of fatigue, NOT clumsy or numb, NOT a limb that is too painful to move) 2. ID which muscles are weak 3. Determine the pattern of weakness (muscle, NMJ, nerve, root, plexus, cord, brain?) 4. Look for associated signs/symptoms (numbness, tingling, painful; reflexes?). Are they consistent with localization? 5. Consider the differential diagnosis of d/o w/in your localization 6. Use lab tests and EMG/NCS if needed a. Blood tests or neuroimaging b. EMG/NCS to further localize problem to a particular segment of the peripheral nervous system Differential Diagnosis of Weakness Anatomic Pattern of Weakness Associated Si/Sx Lab Studies Differential Location Diagnosis Primary Muscle Symmetric, proximal Muscle pain (if Serum CK level is Acquired weakness and can affect neck process is elevated in some d/o (myopathies) d/t muscles (not usually affected inflammatory, e.g. EMG may show inflammatory or toxic in a brain or nerve lesion) polymyositis) characteristic etiology Distal muscles affected later Sensory si/sx are not “myopathic” pattern Congenital (muscular or not as severely present dystrophies) NMJ Proximal weakness; some Sensory si/sx are not EMG/NCS can Myasthenia Gravis can lead to ptosis and present demonstrate nearly Lambert-Eaton weakness of extraocular, ANS features pathognomonic Myasthenic bulbar, and neck muscles sometimes present findings for some d/o Syndrome Fluctuation of weakness is Some d/o have important—degree may specific serum change from hr to hr, may be markers (anti-AChR worse after using muscles or Igs in myasthenia toward end of day and gravis) improve after resting or in the morning (fatiguability) or improve after exercise Peripheral Nerve
  9. 9. Mononeuropathie Weakness of muscles Sensory sxs (e.g. EMG/NCS: confirm Usually occur d/t s innervated by a single numbness, tingling, clinical suspicion of entrapment (e.g. peripheral nerve pain) in distribution of problem w/ peripheral Carpal Tunnel the peripheral nerve nerve Syndrome) Mononeuropathy Certain systemic d/o can lead Characteristically a/w NCS: does the A/w systemic Multiplex to dysfxn of multiple pain pathologic process vasculitis, metabolic, peripheral nerves in involve axons or or rheumatologic d/o succession myelin of the nerve Demyelinating Polyneuropathy Peripheral nerves are all Usually have EMG: relative acuity polyneuropathies can affected diffusely, w/ dysfxn associated sensory or chronicity of d/o be hereditary occurring in longest nerves loss and depressed or (Charcot-Marie- 1st (progression of weakness absent reflexes, Tooth) or acquired from distal to proximal, especially in distal (Guillain-Barre) symmetric) extremities Nerve Root Radiculopathy Dysfxn of single nerve root Pain or tingling EMG/NCS can Herniated discs Polyradiculopathy Dysfxn of multiple nerve radiating out from confirm that nerve Shingles roots back or neck roots are the culprit; Inflammation Objective sensory loss can differentiate b/w Infection rare in d/o of single root v. peripheral nerve root b/c of nerve problem overlap from adjacent MRI (spine): for roots single rad., to r/o If nerve root subserves structural etiologies a particular muscle LP: for polyrad. to stretch reflex, that look for infectious or reflex may be inflammatory depressed or absent processes Plexus Brachial Multiple muscles in a limb Sensory findings (in EMG/NCS: confirms Idiopathic Lumbosacral are weak and do not conform distribution of one or the localization inflammation, to a particular nerve root or more roots or nerves) MRI of brachial or radiation, metastases, peripheral nerve pattern Dropped reflexes lumbosacral plexi to r/ hemorrhage, trauma o mass lesions Diabetic pts characteristic lumbosacral plexopathy (diabetic amyotrophy) Spinal Cord Weakness in UMN pattern Maybe sensory loss MRI (spine): r/o Inflammation (e.g. below lesion, and in a nerve below level of lesion structural etiologies or transverse myelitis) root pattern at lesion level d/t interruption of demonstrate intrinsic Infarction ascending tracts inflammation Compression Reflexes below lesion LP: evaluate ALS (degeneration of are typically increased, infectious or corticospinal tracts and Babinski may be + inflammatory etiology and anterior horn Bladder/bowel cells) incontinence maybe Cerebral Hemisphere: Cognitive signs CT or MRI Stroke, demyelinating Hemispheres/ contralateral side in UMN disease, traumatic Brainstem pattern Left hemisphere: injury, tumor, Parasagittal: contralateral aphasia, apraxia infection leg Lateral hemisphere: arm and Right hemisphere: face neglect, visuospatial Deep hemisphere (e.g. dysfunction internal capsule): legs, arms, and face Brainstem: CN Base of pons: ipsilateral dysfunction face, contralateral arm, leg (crossed signs) b/c
  10. 10. descending motor fibers to face have crossed at that level by those to body have not THE SENSORY SYSTEM Anatomy of Sensory Pathways Modality Tract Somatotopic 1st order 2nd order 3rd order Fiber type Arrangement neuron neuron neuron Pain and Spinothalamic Sacralcervica Synapse at Cross and Cortical Thinly temperature tract l level of travel projections to myelinated Lateralmedial dorsal horn of contralaterally postcentral and spinal cord in STT cortex unmyelinated Terminates in slowly thalamus conducting Proprioception, Dorsal columns Legsarms Travel Axons from fibers (A- vibration, light Mediallateral ipsilaterally nuclei gracilis delta and C) touch Nucleus gracilis in dorsal and cuneatus Heavily- Nucleus cuneatus column cross at lower myelinated A- system medulla to alpha and A- Medial lemniscus Legsarms reaching 2nd form the beta) Lateralmedial order neuron medial at level of lemniscus medulla in nuclei gracilis and cuneatus Facial sensation CNV Terminates in thalamus Examining the Sensory System • Touch wisp of cotton • Pain pin • Joint position sense/proprioception moving great toe up and down, moving object up or down on skin and asking pt the direction of movement • Vibration 128-Hz tuning fork applied to toes and other bony structures • Temperature cold tuning fork Sensory Abnormalities: Terms Paresthesia Abnormal sensation described by pt as tingling, prickling, pins and needles, etc. Dysesthesia Unpleasant sensations triggered by painless stimuli Hyperesthesia Increased sensitivity to sensory stimuli Hypoesthesia Diminished sensitivity to sensory stimuli Allodynia Pain provoked by normally innocuous stimuli
  11. 11. Dissociated sensory Loss of one of sensory systems w/ preservation of another one, e.g. in a central cord syndrome, you loss will get loss of pain and temperature (STT) w/ preservation of light touch, proprioception, and vibration sense (dorsal columns) Negative symptoms Numbness, loss of cold/warm sensation, blindness, deafness (d/t disruption of nerve excitation) Positive symptoms Pain, paresthesias, visual sparkles, tinnitus (d/t excitation or disinhibition) Approach to Pt with Sensory Loss • Recognize sensory abnormality by modality • Judge level at which the abnormality is produced • Establish a diff dx of pathologic processes that can affect the particular modality/sensory system • Establish the cause: primary neurologic disease OR systemic disease Patterns of Sensory Loss According to Localization Site of Lesions Sensory Findings Other Neurologic Examples Abnormalities Peripheral nerve Loss of LT, T, PP, proprioception in Associated weakness in Peroneal neuropathy influenced area muscles innervated by that Median and ulnar nerve; distal muscle neuropathies weakness, atrophy, areflexia (LMN signs) Root Loss of all sensory modalities in a Weakness in a myotomal L5 radiculopathy dermatomal distribution distribution, atrophy, Cervical radiculopathy segmental hyporeflexia Plexus Sensory loss in distribution of 2 or more Muscle weakness that cannot Brachial plexopathy d/t peripheral nerves be localized to a single nerve trauma, inflammation, or root infiltration, etc. Spinal cord Sensory level: bilateral loss of all Paraplegia, tetraplegia; Myelopathy sensory modalities initially areflexia, then Sensory dissociation hyperreflexia below the Central cord syndrome Contralateral hypesthesia and ipsilateral lesion and Babinski sign loss of proprioception (Brown-Sequard (UMN signs) syndrome) Brown-Sequard syndrome Proprioceptive loss and corticospinal tract involvement Saddle anesthesia Brainstem Ipsilateral facial numbness and Alternating hemiplegia; CN Posterior circulation contralateral body numbness findings, INO, ataxia strokes Tumor Thalamus Hemibody anesthesia May have motor findings Lacunar stroke Hemmorhage Posterior limb of Hemibody anesthesia Hemiplegia Lacunar stroke internal capsule Hemorrhage Tumor Cortex All modalities affected on contralateral Sensory neglect Parietal stroke side Agraphesthesia Hemorrhage AVM Psychogenic Hyperesthesia for one modality in one Any Psychogenic (a diagnosis of area w/ anesthesia for another modality exclusion) in same area; changing sensory findings Nonphysiologic sensory level changes (abrupt midline changes, vibration asymmetry over forehead) VERTIGO AND DIZZINESS
  12. 12. “Dizziness” • Vertigo: illusion or hallucination of movement that is usually rotatory, but may be linear • Light-headedness: feeling faint, refers to presyncopal state • Dysequilibrium: sensation of imbalance or unsteadiness usually referable to legs rather than to a feeling inside head Vertigo • D/t acute asymmetry of neural activity b/w L and R vestibular nuclei • Does NOT result from slow unilateral loss of vestibular fxn (acoustic neuroma) or from symmetric bilateral loss of fxn (ototoxic drugs) • Approach to determining etiology o Periodicity/duration of sxs o Positional or spontaneous sxs o Peripheral or central origin  Peripheral tinnitus, hearing loss; accompanying N/V more prominent  Central diplopia, dysarthria, dysphagia, or other sxs of brainstem dysfunction; ability to walk or maintain posture may be more impaired Spontaneous Vertigo: Single prolonged episode Vestibular neuronitis Acute unilateral (complete or incomplete) peripheral vestibulopathy; sudden and spontaneous onset of vertigo, N/V; onset over min-hrs, peak w/in 24 hrs, sxs improve gradually over several days/wks; nystagmust is strictly unilateral and may be suppressed by visual fixation; recovery represents central compensation for loss of peripheral vestibular fxn Labyrinthine concussion Can result from head injury; vertigo sometimes accompanied by hearing loss and tinnitus Infarction of labyrinth, Blood supply to central/peripheral vestibular systems via vertebrobasilar system (posterior and brainstem, or cerebellum inferior cerebellar aa. and superior cerebellar artery) and to inner ear via anterior inferior cerebellar artery (infarction of inner ear sudden onset of deafness or vertigo or both) Brainstem or cerebellar stroke most important diff dx in pts w/ suspected acute vestibular neuronitis; if a central-type nystagmus is present, then cerebellar or brainstem infarction w/ associated CN si/sx, weakness, ataxia, or sensory changes that clearly indicate a central process Spontaneous vertigo: recurrent episodes Meniere’s disease Episodic vertigo w/ N/V; fluctuating, but progressive hearing loss, tinnitus, and a sensation of fullness or pressure in ear; d/t an intermittent increase in endolymphatic volume Perilymph fistula D/t disruption of lining of endolymphatic system; pt reports hearing “pop” at time of a sudden increase in middle ear pressure w/ sneezing, noseblowing, coughing, or straining, which is followed by abrupt onset of vertigo Migraine Positional vertigo: peripheral BPPV (benign positional Episodes precipitated by changes in position such as turning over in bed or looking upward; paroxysmal vertigo) attacks are brief (sec-min), and sxs typically begin after a few seconds’ latency following change in position; d/t freely moving Ca++ carbonate crystals w/in one of semicircular canals; when head is stationary, they settle in most dependent part of canal (posteriorly); w/ head movements, they move slower than endolymph w/in which they lie, and their inertia once the head comes to rest causes ongoing stimulation of the hair cells that results in the illusion of movement (vertigo); Dix-Hallpike test is diagnostic (downbeating and torsional nystagmus); Epley maneuver can be used to remove crystals from posterior canal Syncope • Transient LOC and postural tone d/t brain hypoperfusion o Hypotension d/t cardiac dz o Low intravascular volume o Excessive vasodilation • Presyncopal sxs include: light-headedness, HA, neck pain, blurring of vision, cognitive slowing, buckling of knees • 2 neurologic varieties (both involve ANS dysfunction) o Neurogenic syncope (more common): acute hypotension results from transient failure of ANS cardiovascular control; an acute hemodynamic rxn involving a reflex that is triggered by excessive afferent discharges from arterial (including heart and great vessels) or visceral mechanoreceptors; efferent impulses via vagus lead to cardio-inhibition and vasodepression that result in hypotension and bradycardia  Micturition syncope trigger is rapid emptying of distended bladder
  13. 13.  Carotid sinus hypersensitivity trigger is compression of carotid sinus  Neurocardiogenic syncope vigorous contraction of an underfilled ventricle  Vasovagal syncope trigger is strong emotions or pain o Neurogenic orthostatic hypotension: d/t persistent ANS failure; d/t intravascular volume depletion (dehydration, Addison’s disease) or d/t inability to activate efferent SNS fibers appropriately upon assumption of the upright posture; the underlying pathology is either primary or secondary ANS failure (e.g. d/t diabetic ANS neuropathy), but the hallmark of both is failure to release noradrenaline upon standing; consider contribution of drugs such as diuretics, antihypertensives, vasodilators, and antidepressants; drug management to ameliorate sxs include midodrine and fludrocortisone ATAXIA AND GAIT DISORDERS Ataxia vs. Other Gait Disorders • Ataxia: general term describing manifestations of dz of cerebellum or its connections • Other: NOT ALL ataxia is cerebellar in origin, e.g. de-afferentation resulting from loss of position sense also results in ataxia • THUS: distinguish b/w cerebellar v. sensory ataxia Ataxias General • Vermal lesions truncal/gait ataxia • Hemispheric lesions ipsilateral limb ataxia Si/Sx of Cerebellar Disease • Dysmetria abnormality of range and force of movement; manifests as erratic, jerky movements w/ over- and undershooting the target (limb or ocular dysmetria) • Intention tremor rhythmic side-to-side oscillations of the limb as it approaches the target • Dysdiadochokinesia abnormality of rate and rhythm of movement demonstrated by rapid alternating movement test • Gait ataxia broad-based and unsteady, w/ inability to walk in straight line and tendency to lurch from side to side • Truncal ataxia impaired control of truncal posture; when severe, unable to even site unsupported • Dysarthria slow scanning and monotonous speech • Nystagmus Diseases Disease Etiology Characteristics Ass. Si/Sx Course + Prognosis Cerebellar Hemorrhage/infarction Abrupt onset of Level of arousal may Medical emergency hemmorhage/ vertigo, vomiting, be depressed if 4th infarction inability to walk ventricle is compressed w/ hydrocephalus or if there is pressure on BS Postinfectious Typical b/w ages 2-7 Acute onset of limb Lasts a few weeks, cerebellitis following varicella or and gait ataxia, recovery is usually viral infection dysarthria; severity complete ranges from mild unsteadiness to inability to walk Episodic ataxias Inherited mutations in Brief episodes of Ca++ and K+ channels ataxia, vertigo, N/V Paraneoplastic Underlying Acute/subacute onset MRI usually normal Disease peaks in a cerebellar degeneration gynecologic or small of pancerebellar Anti-Yo, anti-Hu period of weeks then cell lung cancer syndrome w/ truncal, autoantibodies in stabilizes, leaving gait, limb ataxia; serum patient w/ profound dysarthria; ocular disability dysmetria and nystagmus Alcoholic cerebellar Long-standing alcohol Vermis bears brunt of Alcoholic Cessation of drinking degeneration abuse; most common damageprogressive polyneuropathy and supplementation of
  14. 14. cause of acquired gait and truncal ataxia nutrition offer the best cerebellar degeneration evolving over wks-mo (though limited) chance of improving Friedrich’s ataxia AR, inherited, Progressive, affects Loss of reflexes, childhood onset arms>legs; severe spasticity, extensor dysarthria plantar responses, impaired vibration and position sense AD spinocerebellar AD, inherited, onset in Insidious onset of Mild to moderate degenerations young adult life progressive cognitive decline is a D/t trinucleotide CAG impairment of gat and late feature expansion dysarthria in young adult life Miller-Fisher Variant of Guillain- Triad of ataxia, IgG anti-GQ1b Self-limiting Syndrome Barre syndrome areflexia, antibodies in serum of Usually full recovery (mediated by post- ophthalmoplegia >90% infectious immune process) Gait Disorders Gait Disorder Anatomical Description Pathology Location Hemiplegic Brainstem Affected leg is stiff and does not flex at hip; leg is Stroke, tumor, trauma Cerebral circumducted, w/ tendency to scrape floor w/ toes; hemisphere arm is held in flexion and adduction and does not swing freely; the spastic (paraparetic) gait is Paraplegic Spinal cord essentially that of a bilateral hemiplegia; adductor Demylination (MS), tone is increased, and legs tend to cross during transverse myelitis, walking (scissoring gait) compressive myelopathy Bihemispheral Diffuse anoxic injury Akinetic-rigid Basal ganglia Stooped posture; narrow-based, slow, shuffling gait w/ Parkinson’s Disease small steps and reduced arm swing; arms carried flexed and slightly ahead of body; difficulty w/ gait initiation; postural reflexes are impaired and pt may take series of rapid small steps (festination) forward (propulsion) or backward (retropulsion) in an effort to preserve equlibrium Frontal Frontal lobes Flexed posture; feet may be slightly apart; gait Hydrocephalus, tumor, initiation is impaired, and word “magnetic” describes stroke, neurodegenerative d/o difficulty lifting feet off ground; pt advances w/ small, shuffling, and hesitant steps; w/ increasing severity, pt Subcortical may make abortive stepping movements in one place Binswanger’s disease w/o ability to move forward Waddling Hip-girdle Muscular dystrophy, spi9nal weakness muscular atrophy, acquired proximal myopathy Sensory Large-fiber D/t loss of proprioceptive input from feet; cautious, Vitamin B12 deficiency Ataxia neuropathy wide-based gait; slow steps; contact w/ ground is (Slapping) made by heel and forefoot then strikes floor w/ a Dorsal slapping sound (slapping gait); walking on uneven Tabes dorsalis columns surfaces or in dark is especially difficult URINARY AND SEXUAL DYSFUNCTION URINARY Anatomy/Physiology of Continence
  15. 15. Circuit Connections Function Circuit 1 Dorsomedial frontal lobe to M region (pons) Volitional control of micturition Circuit 2 (spino-bulbar- Reflex arc starting in bladder projecting to M region spinal) (pons) w/ outflow connections to PNS sacral spinal motor nuclei Circuit 3 Spinal segmental reflex arc w/ afferents from detrusor muscle to pudendal nucleus and efferent fibers to striated sphincter muscles • Pontine micturition center o Areas  M region stimulation decrease in urethral pressure, then rise in detrusor muscle pressure and voiding; M region projects to sacral cord IML  L region (same level) stimulation contraction of urethral sphincter (storage) o Damage loss of inhibitory control over spinal reflexes (circuit 3) and as bladder distends, micturition reflex is automatically activated w/o pt’s awareness or control, and detrusor hyperreflexia and incontinence occurs • Muscles of micturition o Detrusor (smooth): PNS causes contraction; during filling it is inhibited, during micturition it is stimulated o Internal urethral sphincter (smooth): SNS causes contraction; stim during filling, inh during micturition o External urethral sphincter (skeletal): Somatic motor causes contraction; stim during filling, inh during mic Evaluation of Incontinence Urodynamic studies • PVR (postvoid residual): normal<50mL; if increased implies poor bladder emptying (sphincter dyssynergia, atonic bladder are common neurogenic causes) • Cystometry: gives info re bladder compliance, capacity, volume at 1st sensation and at urge to void; voiding pressure; presence of uninhibited detrusor contractions • Cystourethroscopy: assesses integrity of lower urinary system, and IDs important urethral and bladder lesions • Retrograde urethrography • Neurophysiologic studies: sphincter and pelvic floor EMG Type of neurogenic Capacity Compliance Other Indicates… bladder Spastic bladder Decreased Reduced Uninhibited detrusor UMN problem d/t contractions frontal lobe, pontine, or suprasacral spinal cord lesion Atonic bladder Increased Increased Low voiding pressure LMN problem d/t and flow rate lesion at level of conus medullaris, cauda equina, or sacral plexus, or peripheral nerve dysfunction Type of Description Etiology Clinical Patient Associated si/sx incontinence expressio population n Urge Involuntary loss of Detrusor instability Spastic Strokes, Detrusor-sphincter dyssynergia urine a/w strong (DI) bladder suprasacral (DSD): inappropriate desire to void Detrusor hyperreflexia spinal cord contraction of external sphincter (urgency) (if DI d/t neurologic lesions, MS w/ detrusor contraction problem) urinary retention, vesicourethral reflux, and renal damage Stress Involuntary loss of Weak pelvic floor Multiparous urine during muscles women coughing, sneezing,
  16. 16. laughing, or activities that increase intra- abdominal pressure Mixed Urge + stress Overflow Involuntary loss of Underactive or Atonic urine a/w acontractile detrusor bladder overdistension of (drugs, diabetic bladder; constant neuropathy, lower dribbling spinal cord injury, or radical pelvic surgery that interrups innervation of detrusor) Incontinence in the Neurologic Patient • Stroke and spinal cord disease usually produce an UMN bladder or spastic bladder w/ or w/o sphincter dyssynergia o Supraspinal dz  Stroke  Parkinson’s (40-70%) o Spinal cord dz  Spinal cord injury  Multiple sclerosis (75%) • Small-fiber neuropathies can produce a neurogenic atonic bladder w/ high PVR (risk to upper urinary tract), e.g. as in diabetic neuropathy Treatment of Urinary Incontinence Goals • Preservation of upper urinary tract fxn • Improvement of pt’s urinary symptoms that impair quality of life Treatments Disorder Treatments Urge incontinence (spastic bladder) 1. Anticholinergic agents: Tolterodine (Detrol), Oxybutynin (Ditropan), Propantheline 2. TCAs: imipramine 3. Desmopressin spray/tabs (DDAVP): used to treat diabetes insipidus, but produces a significant reduction in voiding frequency 4. Intravesical capsaicin: for intractable detrusor hyperreflexia; has neurotoxic effect on afferent C fibers that drive volume-determined reflex detrusor contractions Stress incontinence 1. Alpha-adrenergic agonist drugs: Phenylpropanolamine, Pseudoephedrine (these stimulate smooth muscle alpha-adrenergic receptors contraction) 2. Estrogen therapy: adjunctive in post-menopausal women Atonic bladder w/ overflow 1. Crede’s maneuver or valsalva maneuver to empty bladder incontinence 2. Intermittent self-catheterization (mainstay of long-term tx) 3. Pharmacotherapy usually not effective; cholinergic agent bethanecol (stimulates cholinergic receptors, increasing detrusor muscle tone Detrusor dyssynergia 1. Intermittent catheterization 2. Suprapubic catheterizaition 3. Sacral nerve stimulation ERECTILE DYSFUNCTION • Persistent inability to attain or maintain penile erection sufficient for sexual intercourse • 10-20 million American men affected • 80% of cases are biologic or organic in origin Anatomy and Physiology • Pudendal nerve: carries motor and sensory fibers that innervate the penis and clitoris • PNS: o Sacral cord S2-S4, erection
  17. 17. o Local mediators: NO, cGMP primarily released by PNS activity contributing to sustained erection • SNS: cells in spinal cord levels T11-T12 through hypogastric plexus, ejaculation Management • Requires recognizing etiology (neurogenic, vascular, traumatic, endocrine, psychogenic, drugs) and treating underlying cause • Pharmacotherapy: o Viagra (25-100 mg/day, 30-60 min before intercourse): SE include facial flushing, HA o Intraurethral suppositories o Intracavernosal injections of alprostadil (Caverject) HEADACHE AND FACIAL PAIN Pathophysiology • Caused by disturbance/irritation of pain-sensitive structures in head o W/in cranium: blood vessels, meninges, CN V, IX, X (brain parenchyma itself + bone are pain-insensitive) o Outside cranium: periosteum of skull, muscles, nerves, vessels, subcutaneous tissues, eyes, ears, sinuses, mucus membranes • Pain pathway o Irritation of pain-sensitive structure nociceptive input relayed to brain via CN V or upper cervical roots  CNV: dermatomal distribution on face, anterior and middle cranial fossas (thus, painful stimulation of structures in ant/mid fossas referred to eye or front or side of head)  Upper cervical roots: dermatomal on posterior surface of head and neck and ears, posterior fossa (thus, painful stimulation of structures in posterior fossa referred to back of head and upper part of neck) 3 General Classes of HAs • Primary (migraine, cluster, tension) not a/w underlying structural cause • HA a/w serious neurologic dz (brain tumor, meningitis, aneurysm) • HA/pain from structures in skull and face (eyes, sinuses, mouth) History of the Presenting HA Hx Component Example Onset and frequency of pain Location of pain Unilateral cluster, migraine Bilateral tension +/- prodromal symptoms? Scintillating scotoma prior to classic migraine Precipitating factors Alcohol as a trigger for cluster Nitrite-containing food (hot dog/salami), tyramine-containing cheese as migraine trigger Description of pain Lancinating/shooting pain in V2/V3 distribution trigeminal neuralgia (tic douloureux) Unilateral throbbing pain migraine Dull, bandlike or tightening pain tension Sharp, stabbing pain esp. behind one eye cluster Associated sx/neurologic signs N/V migraine, increased ICP d/t hydrocephalus or tumor Photophobia, phonophobia, increased frequency of HA at menstruation migraine Fever meningitis, local infection such as dental abscess Unilateral lacrimation or rhinorrhea cluster Primary Headaches Primary HA Type Male- Age of Type of Pain Associated Si/Sx Treatment Femal Onset e Ratio Migraine F>M Teen Unilateral or bilateral, N/V, photophobia, Prophylaxis: avoid years pulsing or throbbing phonophobia triggers, meds (beta- (w/ aura= ”classic”) Aura is a transient blockers like propranolol, (w/o aura= focal neuro sx Ca++ channel blockers like ”common”) preceding HA; most verapamil, TCAs like
  18. 18. common type is amitriptyline, some visual (flashing lights, anticonvulsants like zigzag lines marching depakote) across visual field); Abortive: simple develop over 5-20 analgesics like min, and last 15 acetominophen, aspirin, min-1 hr; HA usually NSAIDS, ergot alkaloids follows w/in 20-60 and selective 5-HT1 min and lasts 4-72 hrs agonists like sumatriptan Tension F=M Any Bilateral and occipital; Muscle spasm may be Many of those used for age pain is dull and involved migraine bandlike, not throbbing Also, PT, stress management, biofeedback, psychotherapy Cluster M>>F 3rd HAs occur in clusters in Ipsilateral Avoid possible precipitants decade which HA recur conjunctival injection, (e.g. EtOH, strenuous of life cyclically (3-4x/day per lacrimation, nasal exercise) cluster) followed by congestion, and Verapamil for prophylaxis remission; each cluster occasional Horner’s Symptomatic tx includes lasts up to several syndrome inhalation of pure oxygen months and remission (>90% effective); can be mo-yrs sumatriptan and Pain behind one eye or dihydroergotamine can be over lateral part of nose used too Secondary HAs HA Type Etiology Description Associated Si/Sx Diagnosis Treatment Subarachnoid Nontraumatic: Sudden, severe, LOC, vomiting, LP or CT: look Acute control of BP Hemorrhage ruptured aneurysm, “worst HA of my neck stiffness for evidence of for adequate brain bleeding from A-V life” hemorrhage or perfusion, monitoring malformation heme b/d in for vasospasm and CSF acute obstructive hydrocephalus d/t subarachnoid blood Definitive tx: surgical resection or clipping of aneurysm Temporal Subacute Occurs in elderly, Scalp tenderness, Elevated ESR Prednisone in Arteritis granulomatous unilateral or jaw pain during to 100 decreasing doses for (Giant Cell inflammatory bilateral, over chewing (jaw Definitive dx several months and Arteritis) condition involving temporal arteries claudication), made by then continued for branches of external involvement of temporal artery next 1-2 yrs carotid artery, esp. ophthalmic artery biopsy temporal arteries can lead to demonstrating blindness vasculitis Trigeminal Microvascular Facial pain Carbamazepine Neuralgia (Tic compression of syndrome in which Douloureux) trigeminal nerve brief severe electrical shock- like pains occur in distribution of a branch of CNV (2 and 3 most common); most common in middle age and elderly; can be precipitated by movement, a cold breeze, or
  19. 19. tactile stimulation in a trigger zone Idiopathic A/w obesity Women in 2-4th Bilateral visual Acetazolamide (CA Intracranial decades of life sxs: fleeting inhibitor): inhibits HTN loss of visual CSF formation (Pseudotumor acuity, Furosemide Cerebri) scotoma, Oral steroids double vision, Serial LP to decrease perhaps CSF pressure papilledema If tx is ineffective, pts CT/MRI may be left w/ normal permanent visual loss LP shows increased pressure >250 mm water Post-Lumbar Following LP HA in an upright IV caffeine sodium Puncture or position starting w/ benzoate Low-Pressure in 48 hrs of LP and Blood patch HA resolving in several days w/o tx; HA relieved when lying down