Color Atlas of Neurology

Encephalopathies

Microemboli in a patient with bacteremia (Staphylococcus aureus)

Acute alcohol intoxication (uncritical self-assessment, disinhibition)

Central Nervous System

313

Central Nervous System

314

Signal attenuation (pons)

Central pontine myelinolysis

(sagittal/axial T1-weighted MRI images)

Iatrogenic encephalopathy

Inhalation of industrial or household chemicals (“sniffing”)

Ethylene oxide (gas sterilization) Lead (children)

Industrial waste

Organic solvents (hydrocarbons, ketones, esters, alcohols)

Organic tin compounds (wood care products, silicone rubber, thermal insulators)

Pesticides

Mercury

Thallium (rat poison)

Encephalopathies caused by industrial toxins

Drugs (behavioral changes)

Central Nervous System

315

Peripheral Neuropathies

Neuropathy Syndromes

316from nonnoxious stimuli). Damage to rapidly conducting, thickly myelinated A-! fibers causes

paresthesiae such as tingling, prickling (“pins

and needles”), formication, and sensations of tension, pressure, and swelling. Damage to slowly conducting, thinly myelinated A-δ and C fibers (small fiber neuropathy) causes hypalgesia or analgesia with thermal hypesthesia or anesthesia, abnormal thermal sensations (cold, heat), and pain (burning, cutting, or dull, pulling pain).

Motor dysfunction (p. 50). Weakness usually appears first in distal muscles. In very slowly progressive neuropathies, muscles may become atrophic before they become weak, but weakness is usually the initial symptom, accompanied by hyporeflexia or areflexia. The cranial nerves can be affected. Hyperactivity in motor A-α fibers produces muscle spasms, fasciculations, and/or myokymia.

Autonomic dysfunction (p. 146f) can be manifest as vasomotor disturbances (syncope), cardiac arrhythmias (tachycardia, bradycardia, fixed heart rate), urinary and gastrointestinal dysfunction (urinary retention, diarrhea, constipation, gastroparesis), sexual dysfunction (impotence, retrograde ejaculation), hyperhidrosis or hypohidrosis, pupillary dysfunction, and trophic lesions (skin ulcers, bone and joint changes).

! Etiology (Table 54, p. 390)

Polyneuropathies can be hereditary or acquired (see Table 54).

! Diagnosis (Table 55, p. 391)

The diagnosis of a neuropathy is based on the characteristic clinical findings and patient history. Additional diagnostic studies not indicated on the basis of the patient history and clinical findings may produce not only unjustified costs but also confounding data, leading occasionally to misdiagnosis. Studies to be performed as indicated include neurophysiological tests (nerve conduction studies, electromyography), laboratory tests (blood, CSF), tissue biopsy (nerve, skin, muscle), and genetic tests.

Distribution of sensory deficit (examples)

Mees lines (in patient with nephrotic syndrome)

Exogenous noxae

Endogenous disorders

Peripheral Nerve and Muscle

317

Peripheral Neuropathies

Radicular Lesions

318the supraclavicular plexus can either be preganglionic (intradural, inside the spinal canal) or in-

fraganglionic (extradural, extraforaminal, out-

side the spinal canal). Supraclavicular plexopathies are more common than infraclavicular ones.

! Symptoms and Signs

Brachial plexus. Lesions affecting the entire brachial plexus cause anesthesia and flaccid paralysis of the entire upper limb, with muscle atrophy. Lesions of the upper brachial plexus (C5–C6) cause weakness of shoulder abduction and external rotation, elbow flexion, and supination, with preservation of hand movement (Erb palsy). The limb hangs straight down with the hand pronated. A sensory deficit may be found on the lateral aspect of the arm and forearm. Lesions of the lower brachial plexus (C8–T1) mainly cause weakness of the hand muscles (Klumpke–Dejerine palsy); atrophy of the intrinsic muscles produces a claw hand deformity. A sensory deficit is found on the ulnar aspect of the forearm and in the hand. Concomitant involvement of the cervical sympathetic pathway produces Horner syndrome. Erb palsy is more likely to recover spontaneously than Klumpke– Dejerine palsy.

Lumbosacral plexus. Lesions of the lumbar plexus (L1–L4) cause weakness of hip flexion and knee extension (as in a femoral nerve lesion) as well as thigh adduction and external rotation. A sensory deficit is found in the affected dermatomes (p. 36). Lesions of the sacral plexus (L5–S3) cause weakness of the gluteal muscles, hamstrings, and plantar and dorsiflexors of the foot and toes. A sensory deficit is found on the dorsal aspect of the thigh, calf, and foot. Lesions of the lumbar sympathetic trunk cause leg pain and an abnormally warm foot with diminished sweating on the sole.

! Causes

See Table 57, p. 393.

Mononeuropathies (p. 322 f)

Lesions affecting a single nerve tend to occur at certain favored sites and are usually of mechanical origin (compression, hyperextension, transection) (Table 58, p. 394).

Peripheral Neuropathies

Peripheral Nerve and Muscle

319

Peripheral Nerve and Muscle

320

Peripheral Neuropathies

Causes of radicular and pseudoradicular syndromes

Peripheral Nerve and Muscle

321

Peripheral Nerve and Muscle

322

Mononeuropathies in shoulder/arm region

Carpal tunnel syndrome in right hand

Clawhand

Monkey hand