Brown-Squard syndrome

Background Brown-Squard syndrome is an incomplete spinal cord lesion characterized by a clinical picture reflecting hemisection of the spinal cord, often in the cervical cord region. Patients with Brown-Squard syndrome suffer from ipsilateral upper motor neuron paralysis and loss of proprioception, as well as contralateral loss of pain and temperature sensation. A zone of partial preservation or segmental ipsilateral lower motor neuron weakness and analgesia may be noted. Loss of ipsilateral autonomic function can result in Horner syndrome. Anatomy Spinal cord anatomy accounts for the clinical presentation of Brown-Squard syndrome. The motor fibers of the corticospinal tracts cross at the junction of the medulla and spinal cord. The ascending dorsal column, carrying the sensations of vibration and position, runs ipsilateral to the roots of entry and crosses above the spinal cord in the medulla. The spinothalamic tracts convey sensations of pain, temperature, and crude touch from the contralateral side of the body. At the site of spinal cord injury (SCI), nerve roots and/or anterior horn cells also may be affected. Pathophysiology Brown-Squard syndrome results from damage to or loss of ascending and descending spinal cord tracts on 1 side of the spinal cord. Etiology -Traumatic causes Brown-Squard syndrome can be caused by any mechanism resulting in damage to 1 side of the spinal cord. Multiple causes of Brown-Squard syndrome have been described in the literature. The most common cause remains traumatic injury, often a penetrating mechanism, such as a stab or gunshot wound or a unilateral facet fracture and dislocation due to a motor vehicle accident or fall. Prognosis Prognosis for significant motor recovery in Brown-Squard syndrome is good. One half to two thirds of the 1-year motor recovery occurs within the first 1-2 months following injury. Recovery then slows but continues for 3-6 months and has been documented to progress for up to 2 years following injury. The most common pattern of recovery includes the following :

Recovery of the ipsilateral proximal extensor muscles prior to that of the ipsilateral distal flexors Recovery from weakness in the extremity with sensory loss before recovery occurs in the opposite extremity

Recovery of voluntary motor strength and a functional gait within 1-6 months

Symptoms

Hemiparaplegia Hemianesthesia - on the opposite side to the paralysis Paralysis of voluntary muscles below level of lesion Segmental atrophy at level of lesion Sensory loss at level of lesion Contralateral analgesia below lesion Thermanesthesia below lesion Sphincteral disturbances Increased muscle tone at side of lesion Increased deep reflexes Clonus Babinski sign

LOSS OF TWO-POINT DISCRIMINATION Normally, a person should be able to recognize two points separated by as little as 24 mm on the lips and finger pads, 815 mm on the palms and 3040 mm on the shins or back (assuming the points are at the same dermatome).The posterior column-medial lemniscus pathway is responsible for carrying information involving fine, discriminative touch. Therefore, two-point discrimination can be impaired by damage to this pathway or to a peripheral nerve.