Neurologic symptoms/neurological

Deficiency. Macrocytic anemia, megaloblastic anemia, and neurological symptoms characterize vitamin B 2 deficiency. Alterations in hematopoiesis occur because of the high requirement for vitamin B 2 for normal DNA repHcation necessary to sustain the rapid turnover of the erythrocytes. Abnormal DNA repHcation secondary to vitamin B 2 deficiency produces a defect in the nuclear maturational process of committed hematopoietic stem cells. As a result, the erythrocytes are either morphologically abnormal or die during development. 

Neurological symptoms result from demyelination of the spinal cord and are potentially irreversible. The symptoms and signs characteristic of a vitamin B 2 deficiency include paresthesis of the hands and feet, decreased deep-tendon reflexes, unsteadiness, and potential psychiatric problems such as moodiness, hallucinations, delusions, and psychosis. Neuropsychiatric disorders sometimes develop independently of the anemia, particularly in elderly patients. Visual loss may develop as a result of optic atrophy. 

The adverse effects iaclude digestive disturbances, neurological symptoms, and manifestations of allergic responses. As many as half of the patients taking it are iacapacitated by some of these adverse reactions for several hours. Whether these symptoms are caused by hypersensitivity to the dmg, the parasite, or by a manifestation of the disease is not known. Overall, effects are dose-related and transient. 

The a-oxidation pathway is defective in Refsum s disease, an inherited metabolic disorder that results in defective night vision, tremors, and other neurologic abnormalities. These symptoms are caused by accumulation of phytanic acid in the body. Treatment of Refsum s disease requires a diet free of chloro-... 

A seizure is an abnormal behavioral (often motoric) activity caused by abnormal electrical activity of the brain. Seizures can be the symptom of a chronic neurological malfunction, i.e. epilepsy, or can appear as single events, e.g. during fever in infants. 

Neurological effects related to cholinesterase depression occurred in seven children acutely exposed to methyl parathion by inhalation as well as orally and dermally (Dean et al. 1984). The children were admitted to a local hospital with signs and symptoms of lethargy, increased salivation, increased respiratory secretions, and miosis. Two of the children were in respiratory arrest. Two children died within several days of each other. All of the children had depressed plasma and erythrocyte cholinesterase levels (Table 3-2). These effects are similar to those occurring in methyl parathion intoxication by other routes (see Sections 3.2.2.4 and 3.2.3.4). Three adults exposed in the same incident had normal plasma (apart from one female) and red blood cell cholinesterase, and urinary levels of 4-nitrophenol (0.46-12.7 ppm) as high as some of the ill children. 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

HCMV is widespread in the human population. In immunocompetent individuals, the infection is inapparent or associated with mild symptoms. However, HCMV is frequently transmitted perinatally and is the leading cause of neurological disease and hearing loss in congenitally infected newborns, affecting some 8,000 newborns per year in USA alone (Arvin and Alford 1990). Furthermore, following the first 100 days after transplantation, HCMV-induced pneumonia develops in about 50%... 

Indirect evidence indicates that dermal absorption occurs in animals. Calves dusted with a 4% dust formulation of endosulfan had neurological symptoms (tremors, twitching, convulsions) and died within a day after exposure (Nicholson and Cooper 1977). Neurological effects have also been reported in preclipped rabbits and rats after repeated application of endosulfan to the skin (Dikshith et al. 1988 Gupta and Chandra 1975). Dikshith et al. (1988) reported levels of a-, [3-, and total endosulfan in liver, kidney, brain, testes, fatty tissue, and blood 30 days after dermal application of endosulfan. 

Immune reconstitution inflammatory syndrome AIDS on HAART Acute or subacute Worsening or new neurological symptoms in the setting of immune reconstitution Immune mediated... 

The clinical presentation of MM in HIV-infected patients is similar to that in other patients with vasculitic neuropathy (Hoke and Comblath 2004). It is characterized by symptoms and signs of sensory involvement, with numbness and tingling in the distribution of one peripheral nerve trunk. Sequential involvement of other noncontiguous peripheral or cranial nerves progresses over days to weeks. The initial multifocal and random neurologic features may evolve to symmetrical neuropathy (Ferrari et al. 2006). 

Berman NE, Marcario JK, Yong C et al (1999) Microglial activation and neurological symptoms in the SIV model of NeuroAIDS association of MHC-II and MMP-9 expression with behavioral deficits and evoked potential changes. Neurobiol Dis 6 486 98 Biber K, Zuurman MW, Dijkstra IM et al (2002) Chemokines in the brain neuroimmunology and beyond. Curr Opin Pharmacol 2 63-68... 

With attenuated viral vaccines the potential hazards are those associated with reversion of the virus during production to a degree of virulence capable of causing disease in vaccinees. To a large extent this possibility is controlled by very careful selection of a stable seed but, especially with live attenuated poliomyelitis vaccine, it is usual to compare the neurovirulence of the vaccine with that of a vaccine known to be safe in field use. The technique involves the intraspinal inoculation of monkeys with a reference vaccine and with the test vaccine and a comparison ofthe neurological lesions and symptoms, if any, that are caused. If the vaccine causes abnormalities in excess of those caused by the reference it fails the test. 

---