Romberg's sign : A brief note
The Romberg's sign or Romberg's test is a phenomenon named by 19th-century European neurologist, Mortiz Romberg. Initially, this sign was tethered specifically with tertiary syphilis patients who exhibited neurologic signs of late-stage disease referred to as locomotor ataxia, or tabes dorsalis.
When examining a patient's neurological effects from sequelae involving late-stage syphilis, the Romberg sign became a precise test to determine the integrity of the dorsal column pathway of the brain and spinal cord, which controls proprioception. Proprioception is the sense of awareness of the position and movement of the body. Romberg described this sign as a severe postural impairment in a darkroom setting or with eyes closed of patients who had severe damage to the posterior dorsal columns of the spinal cord. Used as a precise clinical tool, the Romberg test is positive if a patient is unable to maintain an upright stance with vision eliminated or in the darkness.
Often the Romberg test can be confused as a sign of cerebellar disease, but instead, this test demonstrates the effects of posterior column disease. The ability to gage true proprioception status can be confounded by the vestibular and vision somatosensory system, which may compensate with vestibular function and vision. The Romberg sign removes the visual and vestibular components that contribute to maintaining balance, and can thus identify specifically a proprioception-related neurologic disease.
Physiology and Disease States Affecting Proprioception
Sensorimotor integration of the body is dually controlled by cerebellar input and the posterior column medial lemniscus tracts. The dorsal columns carry proprioception sense (sense of position and joint sense). Important sensory inputs to maintain balance include three peripheral modalities: vision, the vestibular apparatus, and proprioception.
Another disease state that involves the dorsal column and proprioception disruptive behavior is the late complication of vitamin B12 deficiency, termed subacute combined degeneration of the spinal cord (SCD). This condition is an example of the degeneration of the posterior column pathway due to the disrupted formation of myelin and, thus, nerve transmission through saltatory conduction.
Due to the demyelination, the nerve impulse conduction is disrupted and result in clinical proprioceptive impairment. In addition to the late sequelae of Vitamin B12 deficiency, a clinical state involving the vasculature of the spinal cord can also result in a clinical manifestation such as ataxia and proprioceptive deficit. Posterior cord syndrome is a clinical disease state result from posterior spinal artery infarction. This sequel can involve impairment of vibration sense, proprioception, and loss of reflexes below the lesion with sparing of pain and temperature sensation.
Lastly, in a hemisection of the spinal cord, known as Brown-Sequard syndrome, the posterior column pathway of the spinal cord is usually affected. Most cases of Brown-Sequard syndrome are related to trauma. The classic clinical picture involves ipsilateral hemiparesis, loss of vibration and proprioception, and contralateral loss of pain and temperature.
These disease states mentioned above may all result in ataxia as well as many other physical manifestations. To rule out certain disease states, such as Brown-Sequard syndrome, as the etiology for a proprioceptive deficit, taking a thorough past medical history, including trauma history, by the evaluator is crucial for early goal-directed care