NEUROLOGIC INVESTIGATIONS



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, legs; severe dysarthria |extensor plantar responses, | |

| | | |impaired vibration and | |

| | | |position sense | |

|AD spinocerebellar |AD, inherited, onset in young |Insidious onset of progressive|Mild to moderate cognitive | |

|degenerations |adult life |impairment of gat and |decline is a late feature | |

| |D/t trinucleotide CAG |dysarthria in young adult life| | |

| |expansion | | | |

|Miller-Fisher Syndrome |Variant of Guillain-Barre |Triad of ataxia, areflexia, |IgG anti-GQ1b antibodies in |Self-limiting |

| |syndrome (mediated by |ophthalmoplegia |serum of >90% |Usually full recovery |

| |post-infectious immune | | | |

| |process) | | | |

Gait Disorders

|Gait Disorder |Anatomical Location |Description |Pathology |

|Hemiplegic |Brainstem |Affected leg is stiff and does not flex at hip; leg is circumducted,|Stroke, tumor, trauma |

| |Cerebral hemisphere |w/ tendency to scrape floor w/ toes; arm is held in flexion and | |

| | |adduction and does not swing freely; the spastic (paraparetic) gait | |

| |Spinal cord |is essentially that of a bilateral hemiplegia; adductor tone is | |

|Paraplegic | |increased, and legs tend to cross during walking (scissoring gait) |Demylination (MS), transverse |

| | | |myelitis, compressive myelopathy |

| | | | |

| |Bihemispheral | |Diffuse anoxic injury |

|Akinetic-rigid |Basal ganglia |Stooped posture; narrow-based, slow, shuffling gait w/ small steps |Parkinson’s Disease |

| | |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 initiation is |Hydrocephalus, tumor, stroke, |

| | |impaired, and word “magnetic” describes difficulty lifting feet off |neurodegenerative d/o |

| | |ground; pt advances w/ small, shuffling, and hesitant steps; w/ | |

| | |increasing severity, pt may make abortive stepping movements in one | |

| |Subcortical |place w/o ability to move forward |Binswanger’s disease |

|Waddling |Hip-girdle weakness | |Muscular dystrophy, spi9nal muscular |

| | | |atrophy, acquired proximal myopathy |

|Sensory Ataxia |Large-fiber |D/t loss of proprioceptive input from feet; cautious, wide-based |Vitamin B12 deficiency |

|(Slapping) |neuropathy |gait; slow steps; contact w/ ground is made by heel and forefoot | |

| | |then strikes floor w/ a slapping sound (slapping gait); walking on | |

| |Dorsal columns |uneven surfaces or in dark is especially difficult |Tabes dorsalis |

URINARY AND SEXUAL DYSFUNCTION

URINARY

Anatomy/Physiology of Continence

|Circuit |Connections |Function |

|Circuit 1 |Dorsomedial frontal lobe to M region (pons) |Volitional control of micturition |

|Circuit 2 (spino-bulbar-spinal) |Reflex arc starting in bladder projecting to M region (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): normalM |Teen years |Unilateral or bilateral, |N/V, photophobia, phonophobia|Prophylaxis: avoid triggers, meds |

| | | |pulsing or throbbing |Aura is a transient focal |(beta-blockers like propranolol, |

|(w/ aura= ”classic”) (w/o | | | |neuro sx preceding HA; most |Ca++ channel blockers like |

|aura= ”common”) | | | |common type is visual |verapamil, TCAs like amitriptyline,|

| | | | |(flashing lights, zigzag |some anticonvulsants like depakote)|

| | | | |lines marching across visual |Abortive: simple analgesics like |

| | | | |field); develop over 5-20 |acetominophen, aspirin, NSAIDS, |

| | | | |min, and last 15 min-1 hr; HA|ergot alkaloids and selective 5-HT1|

| | | | |usually follows w/in 20-60 |agonists like sumatriptan |

| | | | |min and lasts 4-72 hrs | |

|Tension |F=M |Any age |Bilateral and occipital; pain |Muscle spasm may be involved |Many of those used for migraine |

| | | |is dull and bandlike, not | |Also, PT, stress management, |

| | | |throbbing | |biofeedback, psychotherapy |

|Cluster |M>>F |3rd decade |HAs occur in clusters in which |Ipsilateral conjunctival |Avoid possible precipitants (e.g. |

| | |of life |HA recur cyclically (3-4x/day |injection, lacrimation, nasal|EtOH, strenuous exercise) |

| | | |per cluster) followed by |congestion, and occasional |Verapamil for prophylaxis |

| | | |remission; each cluster lasts |Horner’s syndrome |Symptomatic tx includes inhalation |

| | | |up to several months and | |of pure oxygen (>90% effective); |

| | | |remission can be mo-yrs | |sumatriptan and dihydroergotamine |

| | | |Pain behind one eye or over | |can be used too |

| | | |lateral part of nose | | |

Secondary HAs

|HA Type |Etiology |Description |Associated Si/Sx |Diagnosis |Treatment |

|Subarachnoid |Nontraumatic: ruptured |Sudden, severe, “worst HA|LOC, vomiting, neck |LP or CT: look for |Acute control of BP for |

|Hemorrhage |aneurysm, bleeding from A-V|of my life” |stiffness |evidence of |adequate brain perfusion, |

| |malformation | | |hemorrhage or heme |monitoring for vasospasm and |

| | | | |b/d in CSF |acute obstructive |

| | | | | |hydrocephalus d/t |

| | | | | |subarachnoid blood |

| | | | | |Definitive tx: surgical |

| | | | | |resection or clipping of |

| | | | | |aneurysm |

|Temporal Arteritis |Subacute granulomatous |Occurs in elderly, |Scalp tenderness, jaw |Elevated ESR to 100 |Prednisone in decreasing |

|(Giant Cell |inflammatory condition |unilateral or bilateral, |pain during chewing (jaw |Definitive dx made by|doses for several months and |

|Arteritis) |involving branches of |over temporal arteries |claudication), |temporal artery |then continued for next 1-2 |

| |external carotid artery, | |involvement of ophthalmic|biopsy demonstrating |yrs |

| |esp. temporal arteries | |artery can lead to |vasculitis | |

| | | |blindness | | |

|Trigeminal Neuralgia|Microvascular compression |Facial pain syndrome in | | |Carbamazepine |

|(Tic Douloureux) |of trigeminal nerve |which 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 tactile stimulation in | | | |

| | |a trigger zone | | | |

|Idiopathic |A/w obesity |Women in 2-4th decades of | |Bilateral visual sxs:|Acetazolamide (CA inhibitor):|

|Intracranial HTN | |life | |fleeting loss of |inhibits CSF formation |

|(Pseudotumor | | | |visual acuity, |Furosemide |

|Cerebri) | | | |scotoma, double |Oral steroids |

| | | | |vision, perhaps |Serial LP to decrease CSF |

| | | | |papilledema |pressure |

| | | | |CT/MRI normal |If tx is ineffective, pts may|

| | | | |LP shows increased |be left w/ permanent visual |

| | | | |pressure >250 mm |loss |

| | | | |water | |

|Post-Lumbar Puncture|Following LP |HA in an upright position | | |IV caffeine sodium benzoate |

|or Low-Pressure HA | |starting w/in 48 hrs of LP| | |Blood patch |

| | |and resolving in several | | | |

| | |days w/o tx; HA relieved | | | |

| | |when lying down | | | |

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