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Diseases » Multifocal motor neuropathy » Diagnosis

Diagnosis of Multifocal motor neuropathy

Multifocal motor neuropathy Diagnosis: Book Excerpts

Diagnostic Tests for Multifocal motor neuropathy: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Multifocal motor neuropathy.

Peripheral Neuropathy: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Diabetes

❑ Alcohol

❑ Vitamin B₁₂ deficiency

❑ Drugs

❑ Carcinomatous

❑ Lead

❑ Guillain-Barré

❑ Tabes dorsalis

❑ Syringomyelia

❑ Polyarteritis nodosa

❑ Amyloidosis

❑ Polymyositis

❑ Pellagra

❑ Arsenic

❑ Porphyria

❑ Wallenberg syndrome

❑ Thalamic lesion

❑ Brown-Sequard syndrome

Diagnostic Approach

Sensory neuropathy symptoms include positive phenomena such as tingling; pins/needles; and burning, cold, or lancinating pain. Physical findings include weakness, fasciculations, atrophy, ataxia, wide-based gait, abnormal sweating, decreased or absent deep tendon reflexes, orthostatic hypotension, hypesthesia surrounded by a zone of hyperesthesia, and vibration or position sense affected before pinprick or temperature sense.

Autonomic neuropathy symptoms include impotence, retrograde ejaculation, diaphoresis, incontinence, urinary retention, constipation, diarrhea, orthostatic dizziness, and flushing. Physical findings include delayed pupillary light response, resting tachycardia, sinus arrhythmia, and orthostatic hypotension.

Sensory loss confined to part of a limb suggests injury to a peripheral nerve, plexus, or spinal root, resulting from trauma, entrapment, or vascular insufficiency. Mononeuropathy multiplex affects multiple nerves over time (e.g., due to diabetes or vasculitis). Polyneuropathy occurs in a stocking-glove distribution starting with the longest nerves, and is due to axonal neuropathy, with a toxic or metabolic origin. Bilaterally symmetrical symptoms are found in polyneuropathy or spinal cord lesions, while unilateral involvement is seen in contralateral disease of the brainstem, thalamus, or cortex.

Injury to large myelinated nerves produces decreased light touch and proprioception with a sensation of “walking on a thick carpet” or imbalance. Injury to medium fibers causes decreased light touch and vibration sense. Injury to small unmyelinated fibers, as occurs in diabetes or amyloidosis, decreases pain and temperature sensation and produces dysesthesias. Disproportionate loss of vibration sense and proprioception compared with pain and temperature sensation occurs with diseases of the dorsal column of the spinal cord (e.g., neurosyphilis, vitamin B ₁₂ deficiency, or multiple sclerosis) and demyelinating polyneuropathy.

Transverse cord lesions produce loss of all modalities below the level of the lesion and a band of hyperalgesia at the level of the lesion. Lateral cord compression is heralded by early sensory changes. Dorsal cord compression affects proprioception and tactile discrimination without pain or temperature loss. Pernicious anemia and tabes dorsalis preferentially affect the dorsal columns.

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Source: Field Guide to Bedside Diagnosis, 2007

Motor Weakness: Differential Overview
(Field Guide to Bedside Diagnosis)

Generalized

❑ Steroid myopathy

❑ Diabetic amyotrophy

❑ Polymyalgia rheumatica

❑ Polymyositis

❑ Myasthenia gravis

❑ Guillain-Barré syndrome

❑ Hyperthyroidism

❑ Muscular dystrophy

❑ Eaton-Lambert syndrome

❑ Metabolic myopathy

Paraparesis

❑ Trauma

❑ Multiple sclerosis

❑ Amyotrophic lateral sclerosis

❑ Guillain-Barré syndrome

❑ Epidural abscess

❑ Subacute combined degeneration

❑ Syringomyelia

❑ Aortic dissection

❑ Hysterical

Diagnostic Approach

Motor weakness should be distinguished from functional weakness due to systemic disease. Patients with true motor weakness will complain of difficulty performing specific tasks or a feeling of heaviness or stiffness in their limbs. Myopathy can be distinguished by proximal weakness (climbing stairs or combing hair), symmetrical distribution, absence of paresthesias and pain, or disturbance of bowel or bladder function. Proximal muscle weakness is more prominent in myopathy, distal weakness in peripheral nerve or anterior horn cell disease. Bulbar weakness, manifest as difficulty speaking and swallowing, is consistent with anterior horn cell disease or neuromuscular junction disorders. Ocular weakness occurs with myasthenia gravis and myotonic or oculopharyngeal dystrophy.

Acute generalized weakness with an onset over hours can be caused by low levels of potassium, calcium, sodium, magnesium, or phosphate; by botulism; or by viral inflammatory myopathy. Spasticity, manifest as increased tone and sudden release (“clasp-knife”), occurs with CNS lesions. Rigidity occurs with extrapyramidal disorders. Functional overlay should be suspected in the presence of ratcheting “give-away” weakness.

Peek sign: Orbicularis oculi weakness is observed on gentle eye closure. After initial complete apposition of the lid margins, they separate within seconds and the white of the sclera peeks through. Ice test: A glove finger filled with crushed ice is placed over the more ptotic eyelid for 2 minutes. An increase in opening of 2 mm or more is a positive result. Quiver eye movements: very fast, small twitch, jerk-like movements of the eyes upon changing the direction of gaze. Unintelligible speech: after prolonged speaking.

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Source: Field Guide to Bedside Diagnosis, 2007