Neuroleptics dementia from

As we shall see, pioneers in the use of antipsychotic drugs almost uniformly cited deactivation as the main clinical effect of neuroleptics. Because of this, clinicians often referred to the neuroleptic effect as a chemical lobotomy (Haase, 1959). Bleuler (1978) observed that longterm neuroleptic use also often dampens the vitality and the initiative of the person (p. 301). He concluded, So we see that long-term maintenance with neuroleptics is fraught with some of the same disadvantages that are ascribed to lobotomies (p. 301). Chapter 5 will discuss permanent cognitive impairment and dementia from these drugs. 

Overall, in relatively young and healthy patients, the cumulative risk of contracting TD when exposed to neuroleptics ranges from 4% to 7% per year during the first several years of treatment. Approximately one-third of the patients will develop this largely irreversible disorder within the first 5 years of treatment. This represents an astronomical risk for patients and should become part of the awareness of all mental health professionals, their patients, and their patients families. Furthermore, we shall find that TD brings with it the additional risk of irreversible cognitive dysfunction and dementia (chapter 5). 

A report found that even small doses of Risperdal (average dose of 1.7 mg/day) produced or worsened acute extrapyramidal reactions in one-third of an elderly population suffering from dementia (Baker, 1996). Among 41 patients, 6 developed new parkinsonism, 5 had a worsening of previous parkinsonism, one developed cervical dystonia, and one developed neuroleptic malignant syndrome while also taking Tegretol and Mellaril. 

Medication adverse effects in general are more likely to develop in the elderly (Nolan et al., 1988). People who are elderly and people suffering from dementia are at extreme risk for many different adverse effects when exposed to neuroleptics. A recent study of administrative data from a health care insurer in the United States examined 959 cases of patients at least 45 years old who had been diagnosed with dementia,... 

Research indicates that typical and atypical neuroleptic drugs increase the vulnerability of neurons to cell death and even kill brain cells and that the risk increases in patients already suffering from brain disorders such as Alzheimer s (chapter 5). Consistent with this, Sechi et al. (2000) reported on a case of NMS following exposure of a patient with familial dementia with Lewy bodies to low doses of risperidone. 

A clinical study of hospitalized drug-treated patients found many suffering from mental deterioration typical of a chronic organic brain syndrome that the researchers labeled dysmentia (Wilson et ah, 1983). Tardive dysmentia consists of unstable mood, loud speech, and [inappropriately close] approach to the examiner. It is probably a variant of hypomanic dementia.1 The mental abnormalities in the study by Wilson et al. (1983) correlated positively with TD symptoms measured on the Abnormal Involuntary Movement Scale. In addition, length of neuroleptic treatment correlated with three measures of dementia unstable mood, loud speech, and euphoria. The authors stated, It is our hypothesis that certain of the behavioral changes observed in schizophrenic patients over time represent a behavioral equivalent of tardive dyskinesia, which we will call tardive dysmentia (p. 188). The tendency in the literature, perhaps in search of a euphemism, has been to use the term tardive dysmentia even when a full-blown dementing syndrome is described. 

Myslobodsky et al. (1985) found that 88% of the TD patients showed complete lack of concern or anosognosia with regard to their involuntary movement (p. 156). The study also found other indications for cognitive deficits in these patients. Myslobodsky (1986) reported emotional indifference or frank anosognosia of abnormal movements in 95% of TD patients. He theorized that the most probable cause was some form of cognitive decline associated with dementia disorder, probably owing to some neuroleptic-induced deficiency within the dopaminergic circuitry (p. 4). In 1993, Myslobodsky pointed out that patients suffer from denial of TD even while they remain able to voice complaints about their other medical problems and symptoms. He postulated at that time that TD patients lose the motor part of their road map of consciousness. ... 

In regard to neuroleptics, we found that pioneers in their use were most straightforward about its brain-disabling effects. We find the same phenomenon with lithium. Cade (1949) indicated that lithium, when used for other medicinal purposes, produced actual mental depression in a variety of patients, not just those suffering from mania or manic depression. The drug enforced a so-called quieting effect on persons he considered schizophrenic (dementia praecox, in his nosology) ... 

In the light of evidence from large, randomized, double-blind trials, the authors of a thorough review of the role of atypical neuroleptic drugs in the treatment of psychosis and agitation associated with dementia have concluded that low-dose risperidone (0.25-1.5 mg/day) can be used as first-line treatment (19). 

---