Hyporeflexia/Peripheral Neuropathy
Hypoactive reflexes are caused by disease between the spinal cord and muscle, typically involving the root, plexus, or peripheral nerves. Reduced reflexes indicate that one or more components of the reflex pathway are abnormal: peripheral nerve, sensory root, anterior horn cells in cord, motor roots, or muscle. Disturbances of any part of the reflex arc may cause hyporeflexia. Reflexes can be reinforced by having patients pull their hands apart or bite down while the reflex is tested (the Jendrassik maneuver). Patients voluntarily tensing their muscles will diminish or extinguish the reflex, and may need to be distracted. Areflexia implies no reflexes, even with reinforcement. Reflexes present only with reinforcement imply an intact reflex pathway and may or may not be abnormal. Consider the following points when confronted with hyporeflexia:
Normally hypoactive reflexes. Occasionally, normal individuals may have hyporeflexia with no other obvious cause. The presence of a reflex with reinforcement and absence of other signs are reassuring.
Delayed relaxation phase of the reflex. This unique hypoactive or “hung up” reflex is classic for hypothyroidism and at times serves as the first clue to this metabolic abnormality. It is best seen in the ankle jerk reflex.
Asymptomatic areflexia with a large pupil. This is a benign syndrome (Adie syndrome), consisting of generalized areflexia with a large pupil that reacts to accommodation but only slowly to direct light.
Myopathy. Muscle disorders may cause hyporeflexia but usually not areflexia. The decrease in reflex is consistent with the degree of muscle wasting and weakness. Remember, weakness from muscle disease is generally more marked proximally (shoulder and hip), whereas weakness from peripheral nerve disease is more marked distally (hand and foot). Neuromuscular junction disorders usually spare the reflexes.
Isolated unilaterally absent reflex. This important sign of disc disease compressing spinal roots can be seen with diseases affecting specific peripheral nerves (see Chapter 10).
Remember, mononeuropathy and plexus injuries, whether traumatic or from tumor, are other important causes of asymmetric reflex loss (see Chapter 10).
Bilateral areflexia is a key sign of neuropathy (discussed later). A patient with no reflexes usually has a neuropathy. Similarly, a neuropathy that is “length-dependent,” in that the part of the nerve furthest from the cell body is most affected, may cause absent ankle jerks as an early sign.
PERIPHERAL NEUROPATHY
Peripheral neuropathies occur in a broad category of diseases, many of which are common and treatable. The key manifestations include bilateral or multifocal hyporeflexia, sensory or motor involvement, and (at times) autonomic dysfunction.
Peripheral neuropathies are characterized in a variety of ways, which may help in establishing their etiology. The temporal profile may be acute, subacute, or chronic. The pattern may be distal or proximal, symmetric or asymmetric, diffuse or multifocal. The nerve fibers involved may be sensory, motor, autonomic, or a combination thereof. The pathology may be axonal (involving the nerve itself), demyelinating (involving the nerve sheath), or a combination. It may be vasculitic (inflammation to the blood vessels supplying the nerve causing nerve injury) or neuronal (involving the cell body). The fiber type may be large fiber (vibration and position sense) or small fiber (pin, temperature, and autonomic involvement).
The history and physical examination often help to establish possible etiologies. For example, a rapidly progressive course with areflexia, vibration loss, and proximal and distal weakness occurring after a viral illness suggests an acute demyelinating inflammatory polyneuropathy. A slow course with distal muscle wasting in the feet, distal pin and vibration loss, and loss of ankle jerks suggests a chronic, axonal sensorimotor polyneuropathy.
ACUTE AREFLEXIA WITH WEAKNESS
Acute areflexia, with weakness and little sensory loss. This is the classic presentation of acute inflammatory demyelinating polyneuropathy (AIDP), or Guillain-Barré syndrome. This may follow a systemic infection or vaccination by days or weeks, or it may occur after an event such as a surgery.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
