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Somatosensory, nerve roots syndromes
Terms in this set (35)
Lesion involves the medial lemniscus, causing contralateral loss of vibration and joint position sense.
Nerve Roots or Peripheral Nerves.
Distal symmetrical polyneuropathy
Causes bilateral sensory loss in a "glove and stocking" distribution, in all modalities.
Transverse Cord Lesion
All sensory and motor pathways are either partially or completely interrupted. There is often a sensory level, meaning diminished sensation in all dermatomes below the level of the lesion
Ipsilateral UMN-type weakness and loss of vibration and joint position, contralateral loss of pain and temperature. Usually starts slightly below the lesion
Central Cord Syndrome small lesions
Small lesions cause bilateral regions of suspended sensory loss to pain and temperature. Lesions of the cervical cord produce the classic cape distribution; however, suspended dermatomes of pain and temperature sensory loss can occur with lesions at other levels as well.
Central Cord Syndrome large lesions
Large lesions cause lower motor neuron deficits at the level of the lesion. In addition, the corticospinal tracts are affected, causing upper motor neuron signs, and the posterior columns may be involved as well. Because the anterolateral pathways are compressed, there may be near complete loss of pain and temperature sensation below the lesion except for in a region of sacral sparing
Posterior Cord Syndrome
Lesions cause loss of vibration and position sense below the level of the lesion. With larger lesions, there may also be encroachment on the lateral corticospinal tracts, causing upper motor neuron-type weakness
Anterior Cord Syndrome
Lesion causes loss of pain and temperature sensation below the level of the lesion, and damage to the anterior horn cells produces lower motor neuron weakness at the level of the lesion. With larger lesions, the lateral corticospinal tracts may also be involved, causing upper motor neuron signs. Incontinence is common because the descending pathways controlling sphincter function tend to be more ventrally located
T/F. In general, for lesions to affect bowel, bladder, or sexual function, bilateral pathways must be involved.
bilateral medial frontal micturition centers
Lesion may result in reflex activation of pontine and spinal micturition centers when the bladder is full. Urine flow and bladder emptying are normal; however, they are no longer under voluntary control, and the individual may or may not be aware of the incontinence
Lesions below the pontine micturition center and above the conus medullaris levels S2 to S4
cause a flaccid, acontractile (atonic) bladder which usually evolves over weeks to months into a hyperreflexic (spastic) bladder. When the bladder is atonic, reflex contractions of the urethral sphincters often persist, resulting in urinary retention and bladder distention. Catheterization is usually necessary.
Lesions of the peripheral nerves, or of the spinal cord at S2 to S4
cause a flaccid areflexic bladder, or significantly impaired bladder contractility resembling an acontractile bladder. Overflow incontinence is often present.
distal symmetrical polyneuropathy, which results in a characteristic glove and stocking pattern of sensory loss. mononeuropathy can affect any cranial or spinal nerve but is most common in CN III and the femoral and sciatic nerves. Onset is usually fairly sudden, and sensorimotor deficits in the nerve distribution may be accompanied by painful paresthesias. There is often partial or complete recovery over the course of weeks to months after onset.
Complex regional pain syndrome/reflex sympathetic dystrophy
characterized by intense local burning pain accompanied by edema, sweating, and changes in skin blood supply.
Guillain-Barré syndrome, also known as acute inflammatory demyelinating polyneuropathy (AIDP)
Presentation is with progressive weakness, areflexia, and tingling paresthesias of the hands and feet, with motor involvement typically much more severe than sensory involvement. Symptoms usually reach their worst point 1 to 3 weeks after onset; recovery occurs over many months.
an immune-mediated disorder in which there are circulating antibodies against the postsynaptic nicotinic acetylcholine receptors at the neuromuscular junction of skeletal muscle cells.
cauda equina syndrome
Sensory loss in an S2 to S5 distribution is sometimes called saddle anesthesia. Involvement of the S2, S3, and S4 nerve roots can produce a distended atonic bladder with urinary retention or overflow incontinence, constipation, decreased rectal tone, fecal incontinence, and loss of erections. It is essential to detect and treat promptly to avoid irreversible deficits.
BRACHIAL PLEXUS, UPPER TRUNK INJURY (ERB-DUCHENNE PALSY)
Common causes include traction on an infant's shoulder during a difficult delivery as well as motorcycle accidents. Damage causes loss of function in C5- and C6-innervated muscles. "waiters tip"
BRACHIAL PLEXUS, LOWER TRUNK INJURY (KLUMPKE'S PALSY)
Common causes include upward traction produced by grabbing a branch during a fall from a tree, thoracic outlet syndrome, and Pancoast's syndrome. Damage causes weakness of C8- and T1-innervated muscles, resulting in hand and finger weakness, and atrophy of the hypothenar muscles, together with sensory loss on the ulnar aspect of the hand and forearm. If the T1 nerve root is damaged proximal to the sympathetic trunk. there may also be an associated Horner's syndrome
thoracic outlet syndrome
the lower brachial plexus is compressed as it passes between the clavicle and the first rib. Symptoms may be increased by raising and external rotation of the arm, which may also decrease brachial arterial pulses
an apical lung tumor (usually non-small cell carcinoma) extends into the lower brachial plexus. In addition to lower-plexus signs (sometimes including Horner's syndrome), the recurrent laryngeal nerve is occasionally involved as it loops downward into the thorax, producing hoarseness. Ultimately, the entire brachial plexus may be invaded, producing a flail, insensate upper extremity.
There is weakness of all foot and ankle muscles and of knee flexion, loss of the Achilles tendon reflex, and sensory loss in the foot and lateral leg below the knee
PERONEAL NERVE PALSY
Foot drop, with weakness of foot dorsiflexion and eversion, and sensory loss over the dorsolateral foot and shin. Most patients recover spontaneously when the mechanical cause is removed. Foot inversion is normally spared because this function can be carried out by the tibialis posterior (innervated by the tibial nerve)
weakness of foot dorsiflexion, eversion, and inversion
The lateral femoral cutaneous nerve (which originates in L2 and L3) can be entrapped as it passes under the inguinal ligament or fascia lata, producing paresthesias and loss of sensation in the lateral thigh. This entrapment syndrome includes no motor involvement or reflex changes.
Tight-fitting shoes can compress the digital nerves, especially of the third and fourth toes, producing patches of numbness and paresthesias.
anterior cord syndrome
Watershed infarction of the spinal cord is typically at the mid-thoracic vulnerable zone
Infarction of the spinal cord is usually due to
anterior spinal artery occlusion.
present with spinal cord dysfunction that develops relatively quickly, over the course of hours to days. MRI often shows T2 bright areas, and CSF has elevated white blood cell count—usually lymphocytic-predominant
Lateral Pons or Lateral Medulla
Lesion involves anterolateral pathways and the spinal trigeminal nucleus on the same side. It causes loss of pain and temperature sensation in the body opposite the lesion, and loss of pain and temperature sensation in the face on the same side as the lesion.
Thalamic Ventral Posterior Lateral (VPL) and Ventral Posterior Medial (VPM) Nuclei or Thalamic Somatosensory Radiations
Deficit is contralateral to the lesion. As with lesions of the primary somatosensory cortex, sensory loss does not begin neatly at the midline, and various subregions may be differentially affected. The deficit may be more noticeable in the face, hand (particularly in the lips and fingertips), and foot than in the trunk or proximal extremities. All sensory modalities may be involved, sometimes with no motor deficit. Larger lesions may be accompanied by hemiparesis or hemianopia caused by involvement of the internal capsule; lateral geniculate; or optic radiations. Lesions of the thalamic somatosensory radiations can also cause contralateral hemisensory loss, which is associated with hemiparesis because of the involvement of adjacent corticobulbar and corticospinal fibers
Lesions of the thalamus can cause severe contralateral pain
an electricity-like sensation running down the back and into the extremities upon neck flexion. Lesions of nerve roots often produce radicular pain that radiates down the limb in a dermatomal distribution, is accompanied by numbness and tingling, and is provoked by movements that stretch the nerve root
carries information from the legs and lower trunk
lateral cuneate fasciculus
carries information from the upper trunk above about T6, and from the arms and neck.
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