Syndrome of Acute Generalized Weakness

Occasionally the pace of a disease is so rapid that by the time the patient is seen in the hospital the weakness has become generalized. The history of the mode of onset and the early course of the disease may not be available or may be confused by inaccurate observations. Therefore, accurate formulation of the problem depends on the examination and on localization of the level of the motor system that is damaged and is producing the weakness (see Table 15-14 ). The first step in the differentiation is to determine whether the patient is in coma. The "locked-in" patient with a basis pontis lesion may initially appear comatose because he cannot move or speak and has lost the ability to make horizontal eye movements. However, the ability to blink and make vertical eye movements is preserved, and one should attempt to establish a communication code using eye blinks. In severe cases of botulism and AIDP, even ocular movements may be totally paralyzed, but no decorticate or decerebrate posturing is present or any hyperreflexia, and there are no Babinski signs to indicate the presence of an intrinsic brain stem lesion.

Another potential source of confusion is the differentiation of AIDP without cranial neuropathy from an acute transferase myelopathy with spinal shock. Interruption of the descending motor tracts due to an acute transection of the spinal cord not only produces a paralysis below the level of the lesion but also causes a loss of all reflex activity. Tendon reflexes are lost, and initially there is no Babinski sign. However, Babinski signs generally appear within a matter of hours to a few days at most, helping to differentiate between the two. Also, in patients with acute transverse myelopathy there is a well-defined sensory level, whereas in those with AIDP there is minimal if any sensory loss, which is generally distal with no sensory level.

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Peripheral Neuropathy Natural Treatment Options

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