CH43: Peripheral Nerves Flashcards by Robert Sarmiento

Differentiate central and peripheral nerve (p. 1310)

Myelin of centrally located fibers: oligodendrocyte
Myelin of peripheral: Schwann cells

Support central:astroyctes
Supprt peripheral: Fibroblasts

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Disease mechanism is producing toxin that directly acts on the membrane of the Schwann cells near the DRG(p. 1311)

Diphteria

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Disease mechanism is occlusion of vasa nerosum (p. 1311)

Polyarteritis nodosa

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Disease mechanism is treponemal meningoradiculitis (p. 1311)

Tabes dorsaleis

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Disease mechanism is combination of toxin with axoplasm of the largest sensory and motor nerves via sulfhydryl bonds (p. 1311)

Arsenic

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Disease mechanism is damaging the microtubular transport (p. 1311)

Vincristine toxicity

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Retrograde changes consisting of swwelling of the cell cytoplasm and marginalization and dissolution of the NIssl substance (p. 1312)

Chromatolysis

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Exception wherein an axonal process is seen presenting as proximal weakness (p. 1312)

Porphyria

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Compare polyneuropathies vs multifocal. (p. 1313)

The multifocal nature of lesions and blocakge of electrical conduction often leads to weakness of proximal limb and muscles before or at the same time as distal parts are affected.

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Disuse vs Denervation atrophy (p. 1313)

In dususe, the muscle does not reduce its size by ore than 25 to 30%.

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As a rule, neuropathies are associated with a reduction or loss of tendon reflexes EXCEPT (p. 1314)

small fiber neuropathies; in which DTR may be retained even with marked loss of perception of painful stimuli.

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Characteristic of sensory ataxic gait (p. 1315)

brusque, flinging, slapping movements

NO NYSTAGMUS, DYSARTHRIA

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Two most frequent manifestation of autonomic failure (p. 1315)

Anhidrosis

Orthostatic hypotension

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Is there dysautonomia in radicular diseases? (p.1316)

No. Because the autonomic fiebrs join the spinal nerves from the sympathetic chain and parasympathetic ganglia more distally.

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Fasciculations and cramps are NOT prominent features in polyneuropathies (they are in anterior horn cell diseases) EXCEPT (p. 1316)

Chronic spinal motor root compression leads to fasciculations or painful spams in the innervated muscles

TREATMENT: Carbamazepine, Phenytoin

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Differentiate an L5 vs peroneal nerve lesion. (p. 1318)

Check INVERSION. If spared, lesion is in the peroneal nerve.

Check sensory:
L5 extends almost up to the knee on the anterior surface of the foreleg
Peroneal: it ends a limited distance above the ankle

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Infections associated with GBS(p. 1321)

C jejuni
Herpes family (CMV EBV HIV)
Campylobacter- Mycoplasmae and Lyme

Not infection: lymphoma and systemic autoimmune

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GBS: Antibody (p. 1323)

acute motor axonal- GM1
PCB- GT1b, GD1a
MFS- GQ1B

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Pathologic findings in GBS (p.1323)

endoneural perivascular lymphocytic infiltrates

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In GBS, the CSF is under normal pressure or contains only a few lymphocytes in all but __%of patients (p. 1323)

`10%

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Very earliest changes in pathology of GBS(p. 1325)

deposition of compleemnt on the innner layer of myelin

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Differentiate Tick paralysis vs GBS (p.1325)

Sensory loss is not a usual feature of tick paralysis and CSFprotein is normal

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MG vs GBS (p. 1326)

The mandibular muscles remain relatively stron in GBS

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Botulism vs GBS (p.1326)

Bradycardia in botulism

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The ability to reach a count of 20 generally corresponds to a vital capacity of greater than (p.1326)

1.5L

Dysautonomia in how many percent of GBS patients (p. 1326)

10%

Bizarre waking dreams or hallucinations after weeks of immobilization (p. 1326)

Oneiric hallucinations

Dose of plasma exchange (p. 1327)

200 to 250ml/kg in 4 to 6 treatments on alternate days; onset less than 2 weeks

Dose of IvIg (p. 1327)

0.4g/kg per day for 5 consecutive days

How many percent of GBS who intiially improve will relapse with treatment (p. 1327)

10%

Differentiate between acute sensory neuronopathy and GBS (p. 1329)

In GBS, there is usually some degree of proximal wekaness and sensory changes do not extend to the face and trunk

Important pathologic change in diphtheria (p. 1330)

segmental demyelination without inflammatory reaction of spinal roots, sensory ganglia, and adjacent spinal nerves Anterior horn cells, axons, peripheral nerves distally and muscle fibers remain normal

Treatment for diphtheria (p. 1330)

Diphtheria antitoxin within 48 hours

This disease is due to a metabolic defect in the liver marked by increased production and urinary excretion of porphobilinogen and porphyrin precurose alpha aminolevulenic acid (p. 1330)

Porphyria

Characteristics of porphyric neuropathy (p. 1330)

``` relapsing nature acute onset abdominal pain psychotic symtoms predominant motor neuropathy- often bibrachial distrubution of weakness truncal sensory loss tachycardia ```

Treatment for porphyria (p. 1331)

IV glucose and IV hematin

Lung tumors polyneuropathy (p. 1332)

Anti-Hu

This carcinoma accoujnts approx 50 percent of cases of paraneoplastic sensorimotor polyneuropathy and 75% of those with pure sensory neuropathy (p. 1333)

Lung Ca

White transverse banding of the nails (p. 1333)

Mee's lines in arsenic

Chronic exposure to lead paint or fumes (p. 1333)

Lead neuropathy

Antineoplastic drugs and neuropathy (p. 1334)

Cisplatin, Carboplatin, Bortezomib - sensory neuropathy and acrodynia and episodic color changes in fiber tips Paclitaxel [ovarian] - sensory neuropathy Vincristine [lymphomas and leukemias] paresthesias

How much pyridoxine to give to prevent neuropathy from INH (p. 1335)

150 to 450mg daily

Most important factor in the development of DM neuropathy (p. 1336)

Duration of diabetes

Isolated involvement of practically all the major peripheral nerves has been described in diabetes but the msot frequently affected are the __ (p. 1337)

femoral sciatic peroneal

Most prominent pathologic finding in DM neuropathy (p. 1338)

loss of myelinated nerve fibers

Persistent hypergycemia inhibits this transport (p. 1339)

sodium- dependent myoinopsitol transport

Treatment for DM neuropathy (p. 1339)

Amitryptilline Duloxitine Gabapentin Pregabalin

Nerve biopsy findings of polyarteritis nodosa (p. 1340)

necrotizing arteritis in medium- size vessles with infiltrating eosinophils and occlusion of vessels TX: Rituximab, Cyclophosphamide

Vasculitis that involves the lungs in contrast to renal and bowel infarctions of Polyarteritis Nodosa (p. 1340)

Churg-Strauss

Finging relatively specific for Wegener and Churg Strauss that helps differentiate with polyarteritis (p. 1341)

circulating c-ANCA TX: Corticosteroids, rituximab, cyclophosphamide

Distinguishes the neuropathy of sarcoidosis from other forms of mononeuropathy multiplex (p. 1343)

`Occurence of large, irregular zones of sesnory loss over the trunk

Triad of Lyme disease (p. 1343)

cranial nerve palsies radiculitis aseptic meningitis

Painful lumbosacral radiculitis of lyme disease (p. 1344)

Bannwarth syndrome - sparing of the proximal or distal part of the limb while the adjacent part is weakend Dx: Western blot Tx:Ceftriaxone 2g for 1 month

Chronic slowly progressive autoimmune disease characterized by lymphocytic infiltration of exocrine glands, particularly of parotid and lacrimal glands hence keratoconjunctivitis and sicca (p. 1344)

Sjogren Disease Tx: Prednisone, Cyclophosphamide, Rituximab

Serologic abnormalities in Sjogren (p. 1345)

AntiRo SSA; Ani La SSB

The defining feature of this unusual syndrome are searing and pulling sensations involving small cutaneous areas that are evoked by exetending or stretching the limb (p. 1346)

Wartenberg syndrome

One exception to the rule that all chronic neuropathies are more or less symmetrical in pattern (p. 1348)

Leprous neuritis

In polyneuropathy with associated paraproteinemia, Roberg sign, propioceptive sensory loss with gait imbalance, tremor are typical fidngins in teh group with ___activity (p. 1349)

Anti-MAG

Hyperviscosity in Walderstrom hyperproteinemia manifesting as diffuse slowign of retianl and cerebral circulations, episodic confusion, coma, impairment of vision and strokes (p. 1350)

Bing- Neel syndrome

Chian in myeloma (p. 1351)

Kappa | Lambda can be in amyloid neuropathy or osteosclerotic type

Pathologic findings in CIPD (p. 1353)

interstitial and perivascular infiltates of inflammatory cells Tx: IvIg, Plasmapharesis, Cyclophosphamide, Mycophenolate mofetil, Rituximab

MMN antibody associated (p. 1355)

Angi-GM1

Description of uremic polyneuropathy (p. 1355)

painless, progressive, symmetrical sensorimotor paralysis of legs and arms

Type of leprosy:epithelioid granuloma that involves cutaneous and subcutaneous nerves and results in characteristic hypopigmented patch of sperficial numbness and sensory loss (p. 1356)

tuberculoid leprosy

Type of leprosy: proliferation of hematogenous spreads of bacilli and the diffuse infiltration of skin, ciliary bodies, testes, lymph nodes and nerves (p. 1356)

lepromatous leprosy

Idiopathic small fiber sensory polyneuropathy gene assocation (p. 1358)

SCN9A encoding voltage gated sodium channel NaV1.7

Most common type of Charcot Marie Tooth (p. 1361)

CMT1A- due to 17p duplication

Muscle deformity due to CMT (p. 1361)

inverted champagne bottle

Difference between CMT1 and CMT2 (p. 1361)

Enlargement of nerves in Type 1, most easily appreciated by palpation of the great auricular and peroneal nerves

Electrographic features of CMT (p. 1361)

slow (less than 38m/s) in CMT1 | normal in CMT2

If slow nerve velocities, check for these genes in CMT (p. 1362)

PMP22, CMTX1

Pathologic findings in CMT (p. 1362)

depletion of population of large sensory and motor fibers, leaving only the condensed endoneural connective tissue

Hereditary Neuropathy with Pressure Palsies vs CMTY (p. 1362)

both PMP22A gene is affected. In CMT1A- gene is duplicated In HNPP- gene is deleted

Hypertrophy neuropathy of infancy (p. 1362)

Dejerine-Sottas Disease

In HSAN1, a consequence of loss of function of this enzyme which is the rate- limiting step in the biosynthesis of sphingolipids (p. 1363)

serine palmitoyltransferase

Symmetrical lipomas of the neck and shoulders that are associated with polyneuropathy and sometimes, deafness (p. 1364)

Launois- Bensaude disease

Familial dysautonomia after birth. Tongue lacks fungiform papillae (p. 1364)

Riley-Day Familial dysautonomia DX: check amounts of homovanillic acid and decreased vanillylmandelic acid and methoxyhydroxyphenylglycol

Retinitis pigmentosa, ataxia, chronic polyneuropathy with increase in blood phytanic acid (p. 1366)

Refsum disease

Finding of red blood cell acanthocyts, low serum cholesterol and b lipoprotein (p. 1366)

Bassen- Kornzweig Syndrome

Mutation elimiantes the function of ATP casette transport protein (p. 1367)

Tangier Disease

alpha-galactosidase deficiency; angiokeratomas, painful neuropathies (p. 1367)

Fabry disease

Metaphyseal dysplasia that resembles acromegaly (p. 1367)

Pyle disease

Amyloid is derived from an inherited abnormality of serum protein __ (p. 1468)

transthyretin

Two novel treatment for amyloid (p. 1369)

Tafamidis | Interfering RNA therapy

Ischemic condition resulting from thrombosis of the subclavian artery or vein (p. 1372)

Paget- Schrotter syndrome

If the denervatin changes are found in the paraspina lmuscles, the source of weaknes and pain is in the intraspinal roots, proximal to the plexus (p. 1372)

TRUE

Nerve damaged in meatpackers neuropathy (p. 1376)

Suprascapular nerve | from carrying objectes on teh shoulder

Sign that consists of hyperflexion of the wrist for 30 to 60s (p. 1377)

Phalen maneuver

lighlty tapping the volar aspect of the rist ast the transverse carpal ligament (p. 1377)

Tinel sign

Uppper vs Lower lumbar plexus (p. 1378)

ULP: weakness of flexion and adduction of the thigh and extension of the leg sensory of anterior thigh and leg LLP weakness of posterior thigh, leg and foot muscles and abolish sensations over the first and second sacral segments

Most common cause of femoral neuropathy (p. 1381)

diabetes

Most frequently compressed nerves in order (p. 1382)

``` median ulnar peroneal tibial plantar ```