[The neuropathy epidemic in Cuba: eight years of investigation and follow-up].

Introduction: The authors describes the past eight years, since an epidemic started in Cuba which mainly affected the nervous system, particularly the optic nerve and the peripheral nerves. It is thought to have been the biggest epidemic involving the nervous system this century, although there may be over-diagnosis. The cause is controversial but is probably nutritional imbalance with additional toxic elements also in some cases.

Optic neuropathies for the neurologist.

Before embarking on expensive ancillary testing, it is crucial for the neurologist to distinguish visual loss due to optic nerve dysfunction from other causes of visual loss. This can usually be accomplished based on specific features of the history and bedside examination. Once it has been established that a patient has some form of optic neuropathy, several clinical features are helpful in determining the etiology.

[Leber's hereditary optic neuropathy and its possible relation to a recent epidemic in Cuba].

Introduction: This century, the greatest epidemic affecting the nervous system was notified in Cuba seven years ago. At the present time the epidemic continues although to a lesser extent. The clinical findings of the illness were mainly bilateral optic neuropathy sometimes accompanied by other symptoms and peripheral neuropathy.

Chiasmopathy?

A 57-year-old man presented with progressive visual loss in both eyes, bitemporal field defect, and a history of poor nutrition, alcohol abuse, and excessive cigar smoking. Magnetic resonance imaging was normal. The visual acuity and field defect improved with supplementation with vitamins and reduction of alcohol and tobacco consumption.

[The eye and nutrition].

Purpose: To examine the effect of vitamins and trace elements on ocular tissue.

Materials And Methods: Rats or mice were fed diets deficient in the trace elements Zn, Cu, Mn, Se, Mg, and Cr or in vitamins A, B12, C, and E. In some rats Al and vitamin A were injected in excessive amounts.

Acquired mitochondrial impairment as a cause of optic nerve disease.

Background: Blindness from an optic neuropathy recently occurred as an epidemic affecting 50,000 patients in Cuba (CEON) and had clinical features reminiscent of both tobacco-alcohol amblyopia (TAA) and Leber's hereditary optic neuropathy (Leber's; LHON). Selective damage to the papillomacular bundle was characteristic, and many patients also developed a peripheral neuropathy. Identified risk factors included vitamin deficiencies as well as exposure to methanol and cyanide.

[Risk factors in the epidemic neuropathy of Cuba].

Objective: A case control study to find out if Cuba's epidemic neuropathy was a result of one of the following causes: (1) an infectious process, (2) exposure to one or more toxical agents, (3) low intake of one or more nutrients, or (4) more than one of such causes and their interactions.

Material And Methods: A total of 311 cases of epidemic neuropathy with optic and peripheral symptoms and 377 controls were studied. A questionnaire with 55 items was employed to document exposure to factors determined by the etiologic hypothesis.

[Clinical characteristics of the peripheral form of epidemic neuropathy in the province of Cienfuegos].

Introduction: From October 1992 to September 1993 clinical observations of the civil population of Cienfuegos revealed the presence of epidemic neuropathy (EN) reaching about 2,000 patients. The clinical manifestations were not uniform. Although numerous studies have been carried out in our country, none have established the characteristics of EN 'the peripheral form'.

[Clinical characteristics of Cuban epidemic neuropathy].

Introduction: At the beginning of 1992 an epidemic neuropathy was seen in Cuba.

Material And Methods: To determine the clinical characteristics we studied the clinical and neurological features, cerebrospinal fluid, and did neurophysiological investigations and sural nerve biopsies.

Results: Sixty patients were studied.

[Mechanism of Enterovirus participation in epidemic neuropathy. Physiopathological hypothesis].

During the epidemic neuropathy occurred in Cuba from 1992 to 1993, viral isolations antigenically connected with Coxsackie viruses were obtained from the cerebrospinal fluid of patients. Virological, epidemiological, toxicologic, nutritional, immunological and histopathological investigations were made. Though the disease was related to toxic and nutritional factors, it has been impossible to identify the cause of the epidemic.

Epidemic optic and peripheral neuropathy in Cuba: a unique geopolitical public health problem.

During 1992 and 1993 an epidemic of optic and peripheral neuropathy affected over 50,000 Cubans. This occurred in the unique setting of a communist country which had a widespread health care network and wherein sudden changes in the economy affected most of the population. Although nutritional factors appeared to play a key role in the pathogenesis of the epidemic neuropathy, viral, toxic, and genetic factors were investigated by Cuban and North American scientists.

Cuban epidemic neuropathy, 1991 to 1994: history repeats itself a century after the "amblyopia of the blockade".

The 1991 to 1994 epidemic of neuropathy in Cuba has been one of the more devastating in recent history, affecting more than 50,000 people throughout the entire country with clinical manifestations of optic and peripheral neuropathy. Although the causes are not entirely clear, it seems that a combination of acute nutritional deficiency and the toxic effects of tobacco and possibly other unidentified toxic substances is involved. The epidemic coincided with the acute worsening of the economic situation on the island following political changes in Eastern European countries and a tightening of the US economic embargo.

The optic nerve.

Recent articles in the scientific literature have described major advances in our understanding of the anatomy and vascular relationships of the optic nerve (cranial nerve II) and of the diagnosis and treatment of a variety of disorders affecting this nerve, including congenital anomalies of the optic disc, dominant hereditary optic neuropathy, anterior and retrobulbar arteritic and nonarteritic ischemic optic neuropathy, optic neuritis, Cuban epidemic optic neuropathy, toxic and nutritional optic neuropathies, radiation-induced optic neuropathy, AIDS-related optic neuropathy, optic neuropathies caused by tumors, and papilledema.

Nutrition and optic nerve disease.

The syndrome characterized by papillomacular bundle damage, central or cecocentral scotoma, and reduction of color vision can be produced by toxic, nutritional, or hereditary causes. Patients who present with such a picture should be evaluated for toxic sources such as tobacco or alcohol use. Nutritional deficiencies must be considered and a good family history should be obtained to explore hereditary factors.

[Case-control study of epidemic optic neuropathy in Cuba, 1993].

The purpose of this study was to identify the risk factors for epidemic optic neuropathy, which occurred in Cuba in 1992 and 1993, as well as to formulate a hypothesis about its etiology. The study sample consisted of 551 pairs of cases and controls matched for age, sex, and area of residence. The cases were patients aged 15 years and over who were diagnosed in April 1993.

Epidemic neuropathy in Cuba: morphological characterization of peripheral nerve lesions in sural nerve biopsies.

More than 50,000 patients were affected in Cuba during an epidemic outbreak of peripheral neuropathy from January 1992 until September 1993. The disease presented as either a retrobulbar optic neuropathy, a predominantly sensory peripheral neuropathy, a dorsolateral myeloneuropathy, or as mixed forms. The morphological findings in sural nerve biopsies from 34 patients with various forms of the disease are presented here.

Epidemic optic neuropathy in Cuba. Eye findings.

Objective: To characterize and establish a clinical definition of the optic neuropathy that appeared in epidemic form in Cuba in 1992 and 1993.

Methods: At the invitation of the Cuban Ministry of Health, Havana, members of ORBIS International and the Pan American Health Organization, assembled teams that traveled to Cuba in May 1993. We were initially briefed by Cuban national experts in the areas of virology, nutrition, toxicology, ophthalmology, neurology, and public health.

Food shortages and an epidemic of optic and peripheral neuropathy in Cuba.

From late 1991 to mid-1993, cases of optic neuropathy of unknown etiology, which first appeared in unusual numbers in a western province of Cuba, spread and multiplied throughout the island. The dominant symptoms changed, becoming increasingly those of peripheral neuropathy. Incidence rates peaked in April 1993.

Visual functions and trace element metabolism in tobacco-toxic optic neuropathy.

Visual functions and nutrition metabolic characteristics were studied in 8 subjects (16 eyes) with tobacco-toxic optic neuropathy (TTON). Their visual functions tested by psychophysical and electrophysiologic methods showed that 1: 1. central vision diminished in 16 eyes, 2.

Bilateral central scotomata due to intracranial tumour.

Bilateral centrocaecal scotomata have been recognised as a sign of intrinsic optic nerve disease, usually associated with hereditary optic neuropathy, and nutritional or toxic amblyopias. This report describes four patients with central scotomata due to intracranial masses, three of whom recovered after surgical intervention. The clinician should be alerted to the association in patients with headaches, other neurological signs, and central visual loss.

Bilateral central and centrocaecal scotomata due to mass lesions.

Unilateral central or centrocaecal scotoma may result from optic nerve compression. However, such defects bilaterally usually indicate non-compressive optic neuropathy of toxic or nutritional, hereditary, or demyelinating origin. Three cases are reported of patients who presented with somewhat atypical bilateral central or centrocaecal scotomata and were found to have suprasellar mass lesions demonstrated by CT scan and confirmed neurosurgically.

Cyanide in human disease: a review of clinical and laboratory evidence.

Experimental cyanide exposure in animals causes demyelination and circumstantial clinical and laboratory evidence suggest that there are human parallels. In Leber's hereditary optic atrophy there appears to be a defect in the conversion of cyanide to thiocyanate because of deficient rhodanese activity. For transmitters of the disease smoking carries the risk of blindness and in the most severely affected patients, there is diffuse neurological disease.

West Indian amblyopia.

A series of 21 patients admitted to St Thomas' Hospital, Medical Ophthalmology Unit, with a diagnosis of West Indian or West African amblyopia is reported. Patients were investigated for haematological, biochemical, serological, and radiological abnormalities and particular attention was paid to dietary history. Patients admitted in recent years also underwent neurophysiological investigations.