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Biomedical subjects

G C Román

Publications and source records attributed to G C Román.

At least 19 recordsLinked to original sources
PubMed2004

Vascular dementia. Advances in nosology, diagnosis, treatment and prevention.

Ischemic or hemorrhagic cerebrovascular disease (CVD) produces injury of brain regions important for executive function, behavior, and memory leading to decline in cognitive functions and vascular dementia (VaD). Cardiovascular disease may cause VaD from hypoperfusion of susceptible brain areas. CVD may worsen degenerative dementias such as Alzheimer disease (AD). Currently, the global diagnostic category for cognitive impairment of vascular origin is vascular cognitive disorder (VCD). VCD ranges from vascular cognitive impairment (VCI) to VaD. The term VCI is limited to cases of cognitive impairment of vascular etiology, without dementia; VCI is equivalent to vascular mild cognitive impairment (MCI). Risk factors for VaD include age, hypertension, diabetes, smoking, cardiovascular disease (coronary heart disease, congestive heart failure, peripheral vascular disease), atrial fibrillation, left ventricular hypertrophy, hyperhomocysteinemia, orthostatic hypotension, cardiac arrhythmias, hyperfibrinogenemia, sleep apnea, infection, and high C-reactive protein. Research on biomarkers revealed increased CSF-NFL levels in VaD, whereas CSF-tau was normal. CSF-TNF-alpha, VEGF, and TGF-beta were increased in both AD and VaD. VaD shows low CSF acetylcholinesterase levels. This condition responds to acetylcholinesterase inhibitors, confirming the central role of cholinergic deficit in its pathogenesis. Evidence strongly suggests that control of vascular risk factors, in particular hypertension, could prevent VaD.

Biomarkers↗
PubMed2002

Defining dementia: clinical criteria for the diagnosis of vascular dementia.

The recognition of cerebrovascular disease (CVD) as a contributing factor and a cause of dementia has led to the development of clinical criteria for vascular dementia (VaD). Due to high specificity, the consensus criteria developed by the National Institute for Neurological and Communicative Disorders and Stroke (NINDS)-Association Internationale pour la Recherche et l'Enseignement en Neurosciences (AIREN) have been used in controlled clinical trials to select patients with pure VaD. VaD is predominantly a subcortical frontal form of dementia with prominent executive dysfunction. In contrast, the criteria of the NINCDS-Alzheimer's Disease and Related Disorders Association (ADRDA) emphasize memory loss as the main feature to distinguish Alzheimer's disease (AD) from VaD and from other forms of dementia. Moreover, CVD may precipitate the clinical expression of AD. Although no criteria have been created specifically for patients having AD with CVD, the ischemic score, the Informant Questionnaire on Cognitive Decline in the Elderly and a history of prestroke mild cognitive impairment (MCI) may be useful for identifying patients with this mixed form of dementia.

Aged↗
PubMed2001

Treatment of myelopathy in Sjögren syndrome with a combination of prednisone and cyclophosphamide.

BACKGROUND: Peripheral neuropathy is a common complication of primary Sjögren syndrome, but central nervous system involvement also occurs and may be the only extraglandular manifestation. Sicca symptoms may also be minimal. Combinations of lesions along with relapses and remissions can suggest multiple sclerosis in the proper clinical setting, making the correct diagnosis elusive. OBJECTIVES: To report a case of progressive transverse myelopathy with previous optic neuropathy in primary central nervous system Sjögren syndrome (CNS-SS), and to review 17 previously reported cases and the patient's responses to various therapies. DESIGN: Case report and literature review. SETTING: University hospital. PATIENT: A 63-year-old Hispanic woman with a 10-month history of progressive spastic paraparesis associated with optic neuropathy and a T10 sensory level. Magnetic resonance imaging demonstrated multifocal, contrast-enhancing lesions in the spinal cord. The patient was diagnosed as having CNS-SS because of the presence of sicca symptoms, abnormal serological test results, and salivary gland biopsy results, which fulfilled San Diego criteria for "definite" Sjögren syndrome. She responded to treatment with a combination of prednisone and cyclophosphamide. CONCLUSIONS: Diagnosis of primary CNS-SS requires a high index of suspicion and specialized clinical testing. Treatment with pulse doses of corticosteroids alone may be suboptimal, but results of treatment with a combination of corticosteroids and either cyclophosphamide or chlorambucil have been encouraging.

Anti-Inflammatory Agents↗
PubMed2000

Spinocerebellar syndrome in patients infected with human T-lymphotropic virus types I and II (HTLV-I/HTLV-II): report of 3 cases from Panama.

Cerebellar symptoms at onset are unusual in HTLV-I/II-associated tropical spastic paraparesis (TSP). A prospective study of neurological disorders in Panama (1985-1990) revealed 13 patients with TSP and 3 with HTLV-I/II-associated spinocerebellar syndrome (HSCS) presenting at onset loss of balance, wide-based stance and gait, truncal instability, and mild leg ataxia (vermian cerebellar syndrome), with absent upper limb dysmetria but with postural tremor, downbeat nystagmus, and dysarthria. In 4-5 years, spinal cord manifestations of TSP developed, including spastic paraparesis, pyramidal signs, bladder and sphincter disturbances. Two patients were infected with HTLV-I and another one, a Guaymi Amerindian woman, with HTLV-II. Magnetic resonance imaging (MRI) demonstrated cerebellar atrophy involving predominantly the superior vermis. Mild axonal peripheral neuropathy in the lower limbs, dorsal column involvement and inflammatory myopathy were found by neurophysiology studies. There are 14 similar cases reported in Japan and Canada, but to our knowledge these are the first documented cases of HSCS in the tropics. A cerebellar syndrome constitutes another form of presentation of HTLV-I/II infection of the nervous system.

Cerebellum↗
PubMed1999

Vascular dementia today.

This decade witnessed a resurgence of interest in vascular dementia (VaD) as an increasingly important cause of senile dementia. Although definitions of dementia in general, and of VaD in particular, are still controversial recent diagnostic criteria for VaD acknowledge that pathogenetic mechanisms different from multi-infarct dementia are important in dementia causation. These include subcortical strokes, mainly lacunes, global hypoxic-ischemic events during acute stroke, and ischemic periventricular white matter lesions of the Binswanger type. These lesions tend to be manifested primarily by alterations of frontal executive function control. The importance of these ischemic vascular lesions in the clinical expression of Alzheimer's disease (AD) in very old subjects has also been recognized. Clinically, VaD may present in two forms: Acute VaD includes large-vessel infarction, and lacunar dementia due to small-vessel disease, including thalamic and caudate strokes. Subacute VaD includes Binswanger's disease (BD), cerebral angiopathy with leukoencephalopathy and CADASIL. The discovery of CADASIL, a genetic form of VaD mapped to chromosome 19 as a mutation of the Notch 3 gene, opened research avenues into the pathogenesis of BD. Finally, epidemiological evidence suggests that it may be possible to prevent VaD--and perhaps degenerative senile dementia--by controlling hypertension and other vascular risk factors. These findings offer hope for prevention of this growing public health problem.

Acute Disease↗
PubMed1998

Epidemic neuropathy in Cuba: a public health problem related to the Cuban Democracy Act of the United States.

In 1992, the USA embargo on Cuba was tightened through the passage of the Cuban Democracy Act (CDA) that explicitly restricts food and medical supplies. The embargo has contributed to cause a number of public health problems in Cuba including: (1) an epidemic of more than 50,000 cases of optic and peripheral neuropathies in 1992-1993, resulting from dietary deficiency; (2) an epidemic of esophageal stenoses in toddlers who inadvertently drank liquid lye as a result of a soap shortage for which liquid lye was substituted; (3) an outbreak of Guillain-Barré syndrome in Havana, in June and July 1994, resulting from water contamination due to lack of chemicals for water treatment to eliminate Campylobacter sp.; (4) outbreaks of self-inflicted disease and injuries caused by rioting among Cubans detained at the US Naval base at Guantánamo Bay, and (5) a decline in medical practice standards and public health indicators in Cuba resulting from the enactment of the CDA, documented by the American Public Health Association in 1993 and confirmed in March 1997 by the American Association for World Health. Despite this evidence, the Cuban embargo remains a politically sensitive subject in the USA, resistant to public health concerns, as evidenced by the recent passage of the Helms-Burton Act. The public health effects of the CDA need to be reviewed with possible revocation or at least modification.

Adolescent↗
PubMed1996

Motor neuron disease on Guam: geographic and familial occurrence, 1956-85.

We investigated the geographic and familial occurrence of motor neuron disease (MND) on Guam, and then considered etiologic hypotheses related to cycad use and metal intoxication. The research was based on 303 Chamorros from Guam and 3 Chamorros from other Mariana Islands, all with MND onset on Guam during 1956-85. Inarajan and Umatac, two southern districts, each had, for both sexes combined, an average incidence rate significantly higher than the corresponding overall rate for Guam. Also, for each sex, geographic patterns of incidence were significantly related to 1) socioeconomic level (men only), 2) cycasin concentrations in cycad flour samples (men and women), 3) iron concentrations in water samples (men and women), 4) silicon concentrations in water samples (men only), and 5) cobalt and nickel concentrations in soil samples (men and women). The MND risk in susceptible sibships was about 7-28 times greater than that in the general population. The cycad hypothesis conforms somewhat better than the metal intoxication hypothesis with the data presented.

Female↗
PubMed1995

On politics and health: an epidemic of neurologic disease in Cuba.

Political decisions may cause disease. During 1992 and 1993, an epidemic of neuropathy in Cuba--largely overlooked by U.S. physicians--affected more than 50,000 persons and caused optic neuropathy, deafness, myelopathy, and sensory neuropathy. Patients with the neurologic disease responded to B group vitamins, and oral vitamin supplementation of the population curbed the epidemic. Dietary restrictions and excessive carbohydrate intake were the immediated cause of the epidemic; however, the primary cause might have been political. Political changes in eastern Europe had major repercussions on Cuba's economy and food supply. In turn, these changes compounded the effects of internal political decisions in the island, leading toward isolationism and economic dependence on the former Soviet Union. Also, for more than 30 years, the United States has maintained an economic embargo against Cuba. In 1992, the U.S. embargo was tightened by the Torricelli amendment (or the Cuba Democracy Act), which prohibited third-country subsidiaries of U.S. companies from trading with Cuba and prevented food and medicines from reaching the island; this amendment produced a virtual economic blockade. Penuries resulting from all these political events resulted in the largest epidemic of neurologic disease in this century. Physicians may need to use their influence to modify political decisions when these decisions result in adverse health consequences. The American Academy of Neurology has issued a plea to encourage physicians and other health personnel to support efforts leading to lifting of the U.S. embargo against Cuba for humanitarian reasons.

Cuba↗
PubMed1995

Motor neuron disease on Guam: temporal occurrence, 1941-85.

Using a case registry, we investigated the temporal occurrence of motor neuron disease (MND) on Guam. MND with onset during 1941-85 was documented in 434 Chamorros and 9 non-Chamorro migrants who had lived on Guam before onset. Increased median age at onset and decreased age-adjusted incidence rates (since the early 1960s) were observed for Chamorros of both sexes. Our evidence about MND on Guam is consistent with: 1) The latent period duration has varied from years to decades; 2) With time, the exposure period or latent period, or both, have lengthened; 3) The high risk of acquiring the condition has been reduced since, at least, the early 1950s, and the most recent years of meaningful risk were the early to middle 1960s; 4) The critical age for acquiring the condition is in adolescence and adulthood; 5) Change of environment from Guam to overseas during childhood resulted in decreased risk of acquiring the condition.

Adult↗
PubMed1995

Tropical neuropathies.

Peripheral neuropathies constitute an important cause of neurological disability in the tropics. The clinical manifestations of tropical peripheral neuropathies are identical to those observed by neurologists elsewhere and their aetiologies are also similar. However, the frequency of occurrence, or prevalence, of the different types of neuropathy is clearly different from that observed in developed nations, ranging from epidemic outbreaks of optic and peripheral sensory neuropathy caused by malnutrition--such as in the outbreak recently observed in Cuba--to the endemic problems of leprosy and HTLV-1 infection. A large variety of plant and animal poisons and industrial neurotoxins frequently affect the peripheral nervous system in warm climates. In addition to their public health importance, tropical neuropathies constitute unexplored natural models of disease worthy of clinical and laboratory studies.

Adult↗