Clinical History

Sensory complaints can be subdivided into positive and negative phenomena. Negative phenomena, hypesthesia or hypalgesia, reflect a loss of sensation on stimulation. Positive phenomena are represented by hyperesthesia and paresthesia. Examples include pain perceived with light stimulation of the skin or a sensation of ants crawling on the skin in the absence of any external stimulation. Negative phenomena generally reflect failure along sensory channels secondary to either conduction block or fiber loss at any site along the sensory axis. Paresthesia or spontaneous pain, however, is most likely due to neural hyperactivity generated ectopically from damaged fibers. M

A number of descriptors may be used by the patient to indicate a sensory loss: numbness, dead weight, prickling, tingling, "pins and needles," aching, tightness, creeping, itching, and burning. It is important to clarify the symptoms with the patient. Such terms as numbness may be used when actually the patient is experiencing weakness or, conversely, the patient is referring to an extremity feeling weak or heavy when indeed there is diminished sensation.

Several historical factors are critical in determining the etiology of a patient's sensory complaints. Chief among these is the distribution of the perceived sensory loss. Localization is the foundation for generating an accurate and complete list of conceivable causes. Some examples of the distribution of sensory loss and typical localizations are listed in T§b.!e,.19:l . The patient should also be asked to describe the temporal presentation, clinical course (static, progressive, stepwise, relapsing/remitting), duration, and severity of symptoms. Any precipitating or provocative factors for the sensory complaints should be noted.

Abnormalities of touch sensation are likely readily recognized by the patient, whereas impairment of vibration is generally not noted by patients because this sensory inflow is not a part of the daily conscious experience. Proprioceptive loss is most likely recognized by the patient as a lack of coordination in the limbs or impairment in gait. An early sign of proprioceptive loss may be unmasked by asking if the patient has difficulty walking or reaching for objects in the dark.

It is important to determine if there are any associated neurological deficits to aid in localization and determination of etiology, such as motor deficits, cranial neuropathies, language deficits, sensory neglect, deep tendon reflex changes, limb or gait ataxia, or autonomic dysfunction.

The presence of any familial history of sensory complaints or conditions causing sensory dysfunction must be investigated. In particular, a determination of the pattern of inheritance of a peripheral neuropathy may greatly aid in making a diagnosis.

TABLE 19-1 -- THE PATTERN OF SENSORY LOSS SEEN IN LESIONS THROUGHOUT THE SENSORY AXIS

Distribution of Sensory Loss

Clinical Diagnosis

Single nerve

Mononeuropathy

Multiple peripheral nerves in a single arm

Infraclavicular brachial plexopathy

Single nerve root

Radiculopathy

Multiple spinal roots in a single arm

Supraclavicular brachial plexopathy

Multiple spinal roots in a single leg

Lumbrosacral plexopathy

Symmetrical distal extremities

Legs > arms

Polyneuropathy (e.g., diabetes)

Arms > legs

Polyneuropathy (e.g., vitamin B,2 deficiency)

Symmetrical proximal extremities

Polyneuropathy (e.g., Tangier disease)

Multifocal peripheral nerve distribution

Mononeuritis multiplex

Multifocal partial nerve distribution

Subcortical white matter (e.g. multiple sclerosis)

Distinct sensory level

Spinal cord lesion

With sacral spanng

Extrinsic cord compression or central cord lesion

Saddle distribution

Conus medullans or cauda equina

Incomplete hemibody

Brain stem

Hemibody

Thalamic lesion

Face and arm sparing leg

Sensory cortex or superficial subcortical white matter

Underlying medical conditions that may predispose the patient to disease of the sensory axis must be explored, with careful attention to past medical illnesses, trauma, toxin exposure, and medications. Patients may present with sensory complaints as their only recognizable manifestation of toxin exposure. Toxic neuropathies secondary to medications or environmental exposure are seldom purely sensory neuropathies; however, TableJ .9-2. lists some medications that may cause a predominantly sensory neuropathy. Although the sensory complaints associated with a toxic neuropathy may vary, pathologically there may be a predilection for involvement of a certain fiber type population.

TABLE 19-2 -- MEDICATIONS CAUSING PREDOMINANTLY SENSORY NEUROPATHIES ALONG WITH THE FIBER TYPE PREFERENTIALLY AFFECTED AS

SEEN ON PATHOLOGIC SPECIMENS

TABLE 19-2 -- MEDICATIONS CAUSING PREDOMINANTLY SENSORY NEUROPATHIES ALONG WITH THE FIBER TYPE PREFERENTIALLY AFFECTED AS

Medication

Affected Pathologically

Almitrine

Large greater than small

Chloramphenicol

Small greater than large

Cisplatin

All fibers

Dideoxyeytidine (ddC)

All fibers

Disulfiram

All fibers

Metronidazole

All fibers

Misonidazole

All fibers

Phenytoin

Large greater than small

Pyndoxine

All fibers

Taxol

All fibers

Thalidomide

Small greater than large

Vincristine

Small greater than large

Almost all predominantly sensory toxic neuropathies due to medications are axonopathic rather than myelinopathic.

Eliminating Stress and Anxiety From Your Life

Eliminating Stress and Anxiety From Your Life

It seems like you hear it all the time from nearly every one you know I'm SO stressed out!? Pressures abound in this world today. Those pressures cause stress and anxiety, and often we are ill-equipped to deal with those stressors that trigger anxiety and other feelings that can make us sick. Literally, sick.

Get My Free Ebook


Post a comment