Here's the part to of what ive recently posted regarding neuropsychiatry: This really will help student nurses and nurses alike in their review in understanding psychiatric nursing. Enjoy and learn:
❍ What are some other terms for “pseudoseizure”?
Conversion reaction, hysteroepilepsy, and nonepileptic seizure (the preferred term).
❍ How can a seizure disorder be distinguished from schizophrenia?
Altered mentation from a seizure tends to be ego-dystonic, and the patient can talk about the symptoms in a detached manner. There is generally no evidence of interictal changes on the mental status examination, and the premorbid social histories are generally good. The seizure disorder is characterized with abrupt rather than gradual alterations in personality, mood, and ability to function that are unresponsive to psychiatric or psychological intervention. The patient generally does not quite meet DSM-IV criteria for schizophrenia.
❍ How can a seizure disorder be distinguished from a panic disorder?
Often a difficult distinction, because both conditions have overlapping symptoms—depersonalization, fear, d´ej`a vu and jamais vu, dizziness, illusions, paresthesias, chills, and flushes, which are in part mediated by a similar underlying limbic dysfunction (the temporal lobe modulates fear, for example) and amenable to similar pharmacologic intervention, i.e., benzodiazepines. However, in panic disorders, consciousness is preserved, an EEG will be normal, there are seldom olfactory hallucinations, family history is usually positive, there are no
automatisms, and a positive response is found not to anticonvulsants but to antidepressants (which would typically worsen complex partial symptoms). In addition, panic attacks usually last longer than seizures, and agoraphobia is a prominent symptom in panic but not seizure.
❍ Is there a particular personality type associated with seizure disorder?
Of the qualities traditionally associated with the “epileptic personality type”—dependency, humorlessness, hypergraphia, hyposexuality, religiosity, viscosity, paranoia, and a preoccupation with philosophical or moral concerns—evidence exists only for hyposexuality, as a reflection of a secondary endocrine abnormality evoked by seizures.
❍ Are seizures associated with aggression?
Aggression during a seizure is very unusual, and when it does occur is typically disordered, uncoordinated, undirected, and associated with restraint or postictal paranoid psychosis.
❍ What strategies can be used in treating psychiatric symptoms associated with a seizure disorder?
Strategies that can be used to treat the neuropsychiatric aspects of seizure disorders include assessment of the social factors that aggravate the seizure disorder; adjustment of the anticonvulsant as necessary to minimize seizures, using monotherapy if possible; use of psychotropic medications to target specific psychiatric symptoms, anticipating interactions, using low initial dosages, and waiting for a response plateau before changing the dose again; targeting psychotherapeutic approaches to specific behaviors or stressors; and finally collaboration with all caregivers.
❍ What are the symptoms of Parkinson’s disease?
Parkinson’s is a progressive, nongenetic disorder that presents with both motor and cognitive symptoms. The motor symptoms typically have an asymmetric onset, and consist of bradykinesia and muscular rigidity, flexion at trunk and neck leading to postural instability, difficulty initiating movements, lack of facial expression, and a 4 to 6 Hz resting tremor. Ninety-three percent of those with Parkinson’s suffer cognitive deficits—reduced verbal fluency and naming difficulties, deficits in visual analysis and constructional praxis, and executive dysfunction similar to frontal lobe syndrome—difficulties in selective attention and set maintenance. Recognition memory is usually unimpaired, but procedural memory shows deficits.
❍ What is the etiology of Parkinson’s disease?
The etiology is unknown, although some hypothesize that it is related to exposure to environmental toxins. The bradykinesia and rigidity can be related to progressive loss of neurons in the substantia nigra. There is reduced
dopamine uptake in the putamen. In addition to dopamine, neurotransmitter abnormalities are found in the somatostatin and CRF systems. There is an increase in the number of muscarinic cholinergic receptors (unlike in Alzheimer’s) but a decrease in nicotinic. Pathology shows Lewy bodies in the locus ceruleus, substantia
nigra, and hypothalamus (in contrast to Lewy body dementia, in which Lewy bodies are found in the cortex also).
❍ What are the neuropsychiatric symptoms in Parkinson’s disease?
Depression occurs in 40% to 60%, often before the onset of motor symptoms, and is unrelated to either the duration or severity of the disease or the response to medications, but is associated with dementia. Parkinson’s depression is characterized more by dysphoria, sadness, irritability, pessimism, and suicidal ideation, less by guilt and self-blame. Actual suicide is rare, unlike in Huntington’s chorea. Psychotic symptoms are common (occurring in up to 50% of patients at some point of the disease) usually as a side effect of anticholinergic medications, but can also occur as a result of mood disturbance, other medications, sleep deprivation, or the dementia associated with Parkinson’s disease. The psychotic symptoms can range in severity from hallucinations that cause no distress to delusional states with agitation and terrifying hallucinations of all types.
❍ What tests can help diagnose Parkinson’s?
PET scans show decreased uptake in the striatum, while CT scan and MRI show decreased volume in the substantia nigra of advanced cases. EEG shows nonspecific slowing.
❍ What percentage of patients with Parkinson’s disease manifest dementia?
From 10% to 40%, the risk rising with age. Other risk factors for dementia in Parkinson’s disease are family history, depression, and motor disability.
❍ What are some treatments for Parkinson’s and its associated neuropsychiatric symptoms?
l-Dopa is a dopamine agonist that can help compensate for the bradykinesia and rigidity, as do anticholinergics, but there is no treatment for the postural instability except for physical and occupational therapy. Antidepressants work normally on Parkinson’s patients, but this population is very sensitive to the anticholinergic, sedating, and orthostatic effects of these drugs. ECT is effective for both the affective and motor symptoms. If antipsychotics must be used, atypicals with minimal extrapyramidal side effects will have the least effect on motor symptoms. Quetiapine and clozapine have been shown to be the most effective in controlling psychotic symptoms in Parkinson’s-related psychosis, while aripiprazole is minimally effective and can exacerbate motor function. Risperdal is generally poorly tolerated in these patients and should be avoided. Whenever the use of atypicals is indicated in patients with Parkinson’s disease, monitoring for neuroleptic malignant syndrome–like symptoms is essential, and can be very difficult to distinguish from baseline symptoms. Again, the use of typical neuroleptics such as haloperidol is generally contraindicated, although may be necessary when agitation becomes a safety issue.
❍ What symptoms can occur as a side effect of treating a patient with Parkinson’s disease?
Anticholinergic drugs, while being the most effective in suppressing the parkinsonian tremor, are also the most prone to induce psychosis. Delusions are usually dose related, frequently persecutory, and preceded by vivid dreams or visual hallucinations. Risk factors for delusions are age and concurrent dementia. Thirty percent of treated Parkinson’s patients will hallucinate fully formed animal or human figures, typically at night and with the hallucinations associated with sleep disturbance. These differ from typical anticholinergic hallucinations in that
they are less threatening, more fully formed, not combined with tactile or auditory stimuli, and not associated with delirium. Delirium occurs in 5% to 25% of patients as a medication side effect, with bromocriptine and pergolide particularly implicated. l-Dopa can cause anxiety.
❍ What is delirium?
Delirium is a pattern of diffuse, reversible cognitive deficits with acute onset, and a waxing and waning course. The deficits can include delusions (20%–70%), perceptual disturbances, mood alterations, language (50%–90%) and thought disorders (95%), sleep/wake disturbance (50%–95%), hallucinations (30%), and psychomotor alterations. Disorientation is common, to time (80%), place (70%), and person (20%). Twenty percent of hospital patients will become delirious, and if elderly, the 1-year mortality will be 40%. Some clinicians distinguish between acute confusional state, a disorder of attention associated with frontostriatal dysfunction, and acute agitated delirium, a disorder of emotion associated with middle temporal gyrus dysfunction, but many patients present with a mixed picture.