neurologic disorders
Numbness
Evaluation of Numbness
Because so many disorders can cause numbness, a sequential evaluation is done. First, the distribution of numbness is used to localize the part of the nervous system that is involved. Then, other clinical features—particularly rate of onset, regularity of symptoms (intermittent or persistent), associated neurologic symptoms and signs, and symmetry—further narrow the differential diagnosis and thus guide further questions and tests to diagnose specific causative disorders. Although in practice certain elements of the history are typically asked selectively (eg, patients with a typical stroke syndrome are not usually asked at length about risk factors for polyneuropathy and vice versa), many of the potentially relevant components of the history are presented here for informational purposes. History of present illnessshould include using an open-ended question to ask patients to describe numbness. Symptom onset, duration, and time course should be ascertained. Most important are The location of numbness Associated neurologic symptoms (eg, paresis, dysesthesias, sphincter dysfunction such as incontinence or retention, dysphasia, visual loss, diplopia, dysphagia, cognitive decline) Possible precipitating causes (eg, compression of an extremity, trauma, recent intoxication, sleeping in an awkward position, symptoms of infection) are sought. Review of systemsshould identify symptoms of causative disorders. Some examples are Back and/or neck pain: Osteoarthritis associated herniated disk or spinal cord compression Fever and/or rash: Infectious neuropathy, infectious radiculopathy, brain infection, or systemic rheumatic diseases Headache: Brain tumor, stroke, or encephalopathy Joint pain: Systemic rheumatic diseases Undernutrition: Vitamin B12 deficiency Excessive intake of high-mercury seafood: Toxic polyneuropathy History of drinking Past medical historyshould identify known conditions that can cause numbness, particularly the following: Diabetes, chronic kidney disease, liver disease, or thyroid disease: Polyneuropathy Infections such as HIV, syphilis, or Lyme disease: Infectious peripheral neuropathy or brain infection Coronary artery disease, atrial fibrillation, atherosclerosis, or smoking: Stroke Cancer (particularly lung cancer): Paraneoplastic anti-Hu subacute sensory or motor neuropathy Osteoarthritis or rheumatoid arthritis: Radiculopathy Family history should include information about any familial neurologic disorders. Medication and drinking history should include use of all medications and substances and occupational exposures to toxins. For example, B6 (pyridoxine) supplements, when taken in excess, can cause a crippling loss of body sensations. A complete Introduction to the Neurologic Examination is done, emphasizing the location and neurologic territories of deficits in reflex, motor, and sensory function. In general, reflex testing is the most objective examination, and sensory testing is the most subjective; often, the area of sensory loss cannot be precisely defined. The most subjective but clinically important finding is the affected sensory level, which could point to a specific area of the spinal cord. In patients with numbness, the following findings are of particular concern: Sudden onset (eg, within minutes or hours) of numbness Sudden or rapid onset (eg, within hours or days) of accompanying weakness Dyspnea Signs of cauda equina or conus medullaris syndrome (eg, saddle anesthesia, incontinence, loss of anal wink reflex) Bilateral neurologic deficits below a spinal segment Loss of sensation on both the face and body (on the same side or opposite side of the body) Numbness of an entire limb Theanatomic pattern of symptomssuggests the location of the lesion but is often not specific. In general, Numbness of part of one limb: Peripheral nervous system lesion Hemibody numbness (with or without the trunk): Brain lesion Bilateral numbness below a specific dermatomal level: Transverse myelopathy (a spinal cord lesion) Bilateral numbness not corresponding to a specific dermatomal level: Polyneuropathy, multiple mononeuropathy, or a patchy spinal cord or brain disorder More specific localizing patternsinclude the following: Stocking-glove distribution: When motor signs are minimal or absent, usually an axonal polyneuropathy; when accompanied by weakness and spasticity (eg, hyperreflexia, increased tone, extensor plantar response), sometimes cervical spondylosis or a demyelinating polyneuropathy or demyelinating lesion of the spinal cord Single dermatomal distribution: Nerve root lesion (radiculopathy) Single extremity with more than one nerve or nerve root affected: Plexus lesion (plexopathy) Multiple related or unrelated peripheral nerves: Multiple mononeuropathy Loss of sensation affecting position and vibration disproportionately: Dysfunction of the dorsal columns or a demyelinating peripheral neuropathy Saddle area distribution: Conus medullaris syndrome or compression of the cauda equina (cauda equina syndrome) Crossed face-body distribution (ie, face and body affected on different sides): Lower brain stem lesion Ipsilateral face and body distribution: Upper brain stem, thalamic, or cortical lesion Bilateral numbness in a cape-like distribution over the neck and shoulders: Central cervical spinal cord abnormality, typically a syrinx Findings that indicate involvement of multiple anatomic areas (eg, both brain and spinal cord lesions) suggest more than one lesion (eg, multiple sclerosis, metastatic tumors, multifocal degenerative brain or spinal cord disorders) or more than one causative disorder. Therate of symptom onsethelps suggest likely pathophysiology: Nearly instantaneous (usually seconds, occasionally minutes): Ischemic or traumatic Hours to days: Infectious or toxic-metabolic or autoimmune (eg, multiple sclerosis) Days to weeks: Infectious, toxic-metabolic, or immune-mediated Weeks to months: Neoplastic, or degenerative, or occasionally infectious due to chronic central nervous system (CNS) infection (eg, fungal infection) Degree of symmetryalso provides clues. Highly symmetric involvement: A systemic cause (eg, a metabolic, toxic, medication- or substance–related, infectious, or postinfectious cause; vitamin deficiency) Clearly asymmetric involvement: A structural cause (eg, tumor, trauma, stroke, peripheral plexus or nerve compression, a focal or multifocal degenerative disorder) After location of the lesion, rate of onset, and degree of symmetry have been determined, the list of potential specific diagnoses is much smaller, so that focusing on clinical features that differentiate among them is practical (see table). For example, if initial evaluation suggests an axonal polyneuropathy, subsequent evaluation focuses on features of each of the many possible medications, toxins, and disorders that can cause these polyneuropathies. Testing is required unless the diagnosis is clinically obvious and conservative treatment is elected (eg, in some cases of carpal tunnel syndrome, for a herniated disk or traumatic neuropraxia). Test selection is based on anatomic location of the suspected cause: Peripheral nerves or nerve roots: Nerve conduction studies and electromyography (electrodiagnostic testing) Plexuses: Nerve conduction studies and electromyography and sometimes contrast MRI Brain or spinal cord: MRI Electrodiagnostic tests can help differentiate between neuropathies and plexopathies (lesions distal to the nerve root) and more proximal lesions (eg, radiculopathies) and between types of polyneuropathies (eg, axonal and demyelinating, hereditary and acquired). If clinical findings suggest a structural lesion of the brain or spinal cord or a radiculopathy, MRI is usually indicated. CT is usually a second choice but may be particularly helpful if MRI is not available soon enough (eg, in emergencies). After the lesion is localized, subsequent testing can focus on specific disorders (eg, metabolic, infectious, toxic, autoimmune, or other systemic disorders). For example, if findings indicate a polyneuropathy, subsequent tests typically include complete blood count (CBC), electrolytes, renal function tests, rapid plasma reagin test, and measurement of fasting plasma glucose, hemoglobin A1C, vitamin B12, folate, thyroid-stimulating hormone, and usually serum immunoelectrophoresis and serum protein electrophoresis (particularly if the neuropathy is painful). Serum immunoelectrophoresis and serum protein electrophoresis can help diagnose multiple myeloma. 