Dementia neuroleptics

McShane R, Keene J, Gedling K et al. (1997) Do neuroleptic drugs hasten cognitive decline in dementia Prospective study with necropsy follow up. BMJ 314(7076) 266-270 Mortimer AM, Shepherd CJ, Rymer M et al. (2005) Primary care use of antipsychotic drugs an audit and intervention study. Ann Gen Psychiatry 4 18 DOI 10.1186/1744-859X-4-18 Mulsant BH, Pollock BG, Kirshner M et al. (2003) Serum anticholinergic activity in a community-based sample of older adults relationship with cognitive performance. Arch Gen Psychiatry 60(2) 198-203... 

Increased mortality in elderly w/ dementia-related psychosis Uses Schizophrenia Action Dopamine serotonin antagonist Dose Adults. 10-15 mg PO daily 5.25-15 mg for acute agitation Caution [C, -] Disp Tabs, inj SE Neuroleptic malignant synd,... 

Dementia with Lewy bodies, Parkinson s disease and neuroleptic sensitivity... 

Risperidone is a selective antagonist of both D2 and 5-HT2 receptors. It is currently the neuroleptic leader in the treatment of schizophrenia and of dementia. 

Atypical neuroleptics have a better side-effect profile, and several studies have confirmed their efficacy. Risperidone has been found effective in the treatment of dementia in patients with agitation (N. Hermann et al. 1998 Jeanblanc and Davis 1995 Jeste et al. 1996 I. R. Katz et al. 1999 Lavretsky and Sultzer 1998), in patients with Lewy body disease (Geizer and Ancill 1998), or in patients with L-dopa-induced hallucinations (Meco et al. 1994). Risperidone has better tolerability than classic neuroleptics such as thioridazine and haloperidol (Frenchman and Prince 1997). No studies of the efficacy of olanzapine in the treatment of agitation in patients with dementia have been done, but its use is widely advocated. 

Narayan M, Nelson JC. Treatment of dementia with behavioral disturbance using divalproex or a combination of divalproex and a neuroleptic. J Clin Psychiatry 1997 58 351-354. 

Sunderland T, Silver MA. Neuroleptics in the treatment of dementia. Int J Geriatr Psychiatry 1988 3 79-88. 

Some maintain that rather than treating a disease or condition, neuroleptics often create another disease. Although these drugs eliminate or reduce the intensity of psychotic experiences such as delusions and hallucinations, the adverse side effects that may actually worsen the symptoms of dementia. 

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. 

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). 

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. 

Neuroleptic-Induced Neurotoxicity, Brain Damage, Persistent Cognitive Deficits, Dementia, and Psychosis... 

Consistent with Bonelli et al. s biochemical finding, Alzheimer patients given the newest neuroleptics have a significantly greater loss of autobiographical memories than untreated patients (Harrison Ther-rien, 2007). Put simply, neuroleptics worsen Alzheimer s dementia. 

A number of the CT scan studies have found a correlation between atrophy and persistent cognitive deficits or frank dementia in these neuroleptic-treated patients (DeMeyer et al., 1984 Famuyiwa et al., 1979 Golden et al., 1980 Johnstone et al., 1976 Lawson et al., 1988). Some of these studies used the Nebraska and Halstead-Reitan batteries, considered among the most sensitive for detecting brain damage and dysfunction. 

Many clinical studies have now confirmed the existence of persistent cognitive deficits and dementia in association with neuroleptic use. However, to some extent, researchers have lost their enthusiasm for demonstrating over and over again that neuroleptics cause cognitive deficits, and textbooks of psychiatry simply do not want to mention it (e.g., Hales et al., 2003). This is reminiscent of the history of research into the brain-damaging effects of shock treatment (chapter 9). When repeated... 

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. ... 

Chapter 3 documented that the neuroleptics can produce acute depression and psychosis. This chapter has documented the existence of tardive dysmentia and tardive dementia as well as tardive behavioral abnormalities in children. There is further evidence that the neuroleptics can... 

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