Dr. Henry Strachan, a medical officer working in Jamaica in 1887, described a constellation of symptoms consisting of optic neuropathy, sensorineural hearing loss, peripheral neuropathy, skin and mucous membrane lesions, and numbness, cramping, and burning pain in the hands and feet.These symptoms were also described by Madan during the last Cuban war for independence in 1898; as such, efforts have been made to rename this disease Strachan-Madan syndrome. Strachan’s Disease is understood to be related to generalized malnutrition or specific vitamin deficiencies, although the specific vitamins involved remain unclear.Numerous reports describe these symptoms in malnourished prisoners of war. Strachan’s disease was also described in Cuba in the 1990s, which was linked to group B vitamin deficiencies. 
Strachan described numbness, cramps in the hands and feet, warmth, hyperemia, and severe burning pain in the palms of the hand and soles of the feet, muscle wasting in the hands and feet, vision loss, hearing loss, facial nerve palsies, desquamating skin lesions of the eyelids, lip borders, and nostrils, and monoplegias.
Strachan’s Disease presents similarly to Tropical Ataxic Neuropathy (TAN). Both present with numbness, vision loss, and muscle cramping in the hands and feet. However, Strachan’s Disease may also present with severe burning pain in the hands and feet. Additionally, TAN presents with gait ataxia. While Strachan’s Disease patients may have gait abnormalities, this is due to muscle atrophy rather than sensory gait ataxia.
Specific nutritional neuropathies should be considered in malnourished patients presenting with peripheral neuropathy, vision loss, or sensorineural hearing loss. Deficiencies of thiamine, pyridoxine, nicotinic acid, and riboflavin are known to cause neurologic symptoms.
Another differential diagnosis is HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis (HAM-TSP), a progressive neurological disease caused by Human T-Lymphotrophic Virus 1 (HTLV-1). Clinical features include bilateral or unilateral lower limb weakness, hyperreflexia, spasticity, urinary incontinence, and gait abnormalities. Patients may also present with neuralgias, paresthesias, uveitis, arthritis, polymyositis, and infectious dermatitis. Patients with clinical suspicion of Strachan’s Disease should be screened for HAM-TSP via enzyme-linked immunoassay for detection of HTLV-1 antibodies.
Patients should receive a full neurological workup including neuroimaging and CSF analysis to exclude other disease processes including multiple sclerosis (MS).
Treatment consists of dietary management to improve nutrition status and correct specific nutritional deficiencies. Patients should receive early supplementation with B-complex vitamins and vitamin A. Most case reports show symptom resolution with intravenous nutrition therapy. Rarely, patients may have persistent optic neuropathy after treatment.
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