Here is again another installment to one of my favorite subjects in nursing which is psychiatric nursing.. I wanna help those aspiring students out there who want to be a nurse in the future. I hope this will help you learn more about your chosen profession:
❍ What percentage of brain tumors will cause psychiatric symptoms?
Fifty to eighty percent.
In 20%, the psychiatric symptoms are the first indicator that a tumor exists. Of psychiatric patients, between
0.1% and 3% will have a brain tumor.
❍ What is the most common psychiatric presentation of a brain tumor?
Apathy, depression, irritability, agitation, and an altered level of consciousness—all caused by an increase in intracranial pressure. Often, tumors will cause an exaggeration of previous character traits and coping styles.
Delusions caused by tumors are typically less complex than those characteristic of schizophrenia, and hallucinations are more often visual than auditory. Left-sided tumors are associated with depression and akinesia, while right-sided tumors present with euphoria and an underestimation of the seriousness of the illness. Focal neurologic signs are
❍ Does the psychiatric presentation depend on the type of tumor?
Rapidly growing tumors tend to cause severe, acute agitation or psychosis with associated cognitive dysfunction, while slow-growing tumors tend to present with vague personality changes, apathy, and depression, often without cognitive dysfunction. Tumors with multiple foci are associated with a greater frequency of psychiatric symptoms. Gliomas often present with psychiatric symptoms because they are fast growing with multiple foci, as do meningiomas, which are slow growing but often found in the frontal lobes where they interfere with higher-level
cognitive functions while producing few focal signs. Supratentorial tumors are twice as likely as infratentorial to produce psychiatric symptoms.
❍ What are the most important factors that predict a psychiatric presentation of brain tumor?
Important factors include the extent of the tumor, rapidity of growth, and the propensity for increased intracerebral pressure. Also important, but less so, are the patient’s past psychiatric history, prior level of functioning, and coping
mechanisms. Least important is the location of the lesion.
❍ What are the most common psychiatric presentations of frontal lobe tumors?
Irresponsibility, childishness, indifference toward others, disinhibition, facetiousness, inappropriate sexual behavior, and witzelsucht—a tendency to make light of everything, albeit with a sarcastic, angry edge to the humor. Previous
cognitive skills are preserved and formal intelligence is unaffected, but “executive functioning” can be severely disrupted. Right frontal damage is associated with euphoria; left frontal damage with akinesia, abulia, and flattened
❍ What percentage of frontal lobe tumors present with psychiatric symptoms?
❍ What is the most common psychiatric presentation of temporal lobe tumors?
Cancer in the temporal lobes often presents with a schizophrenia-like illness, but can also cause depressed mood, apathy, irritability, euphoria and hypomania (because of interference in the connections between the temporal and frontal lobes/limbic system), lability and intensification of premorbid personality traits, anxiety, and panic attacks.
❍ How can temporal lobe tumors be distinguished from schizophrenia?
Temporal lobe tumors will often be associated with visual, olfactory, and tactile hallucinations as well as auditory hallucinations, while affect is typically spared. The psychosis will usually present as repeated “spells,” staring
behavior or dreamlike episodes, and there can also be episodic mood swings. Tumors in the dominant lobe are associated with receptive aphasia or deficits in the ability to learn and remember verbal information; those in the nondominant lobe with disruption in the discrimination of nonspeech sounds.
❍ What is the psychiatric presentation of parietal lobe tumors?
Symptoms of parietal lobe tumors are often more cognitive than behavioral. There is often a marked lack of awareness of deficits or even frank denial on the part of the patient (anosognosia or “neglect syndrome”), and the often-bizarre neurologic presentation can lead to incorrect diagnoses of conversion or somatization
❍ How about occipital tumors?
Also fairly silent psychiatrically, fewer than 20% of occipital tumors have an initial behavioral presentation. The characteristic visual hallucinations tend to be simple and unformed, often little more than flashes of light, but can be associated with agitation, irritability, fatigue, suspiciousness, and prosopagnosia (an inability to recognize familiar faces). Homonymous hemianopsia is common.
❍ What is the psychiatric presentation of diencephalic tumors?
Tumors of the thalamus, hypothalamus and the area surrounding the third ventricle often interrupt the cortical–striatal–pallidal–thalamic–cortical loop, affecting many frontal functions and presenting as a frontal lobe syndrome. Hypothalamic tumors can cause hyperphagia, daytime somnolence, or anorexia nervosa. Diencephalic
tumors often cause a subcortical dementia affecting memory and causing slowing of thought processes, apathy, abulia, depression, and inability to manipulate acquired knowledge. Interruption of CSF flow by tumor growth can cause hydrocephalus and consequent generalized cognitive dysfunction.
❍ What are the five signs that should lead one to suspect a brain tumor in a psychiatric patient?
Seizures, especially if focal or new onset (this is the initial manifestation of 50% of brain tumors), headaches (especially if dull, new onset, poorly localized, nocturnal or positional, present on awakening, and worsening with time), nausea and vomiting, sensory changes (especially visual changes, vertigo, or unilateral hearing loss), and focal neurological signs (such as weakness, ataxia, or localized sensory loss).
❍ What procedures may aid the diagnosis of a brain tumor?
CT scans are good for identifying small soft-tissue mass lesions and concomitant calcifications, obstructive hydrocephalus, and midline shift. They may not reveal very small tumors, however, and can miss isodense tumors and carcinomatosis (diffuse meningeal involvement). MRIs have better resolution and are thus better at revealing very small tumors; the drawbacks are cost, the inability to detect calcifications, and the restriction of subjects to those without metal in their heads. Cisternography, in which dye is injected into the ventricles, can aid in the
differential diagnosis of intraventricular tumors and tumor-associated hydrocephalus. Skull x-rays can diagnose craniopharyngiomas, pituitary tumors, and “empty sella” syndrome, but bone scans are better at detecting bony metastases. Chest x-rays are useful for detecting primary neoplasms of the lung, the most frequent source of brain metastases. A lumbar puncture is useful only for diagnosing meningeal carcinomatosis or leukemia if other tests are unrevealing, and requires a preliminary CT scan or MRI if there is any suspicion of increased intracerebral pressure. EEGs are frequently normal, but sometimes there are diffuse or focal spikes or slow waves, either continuous or paroxysmal. Angiography is useful for establishing the vascular supply of a tumor prior to surgery. Neuropsychiatric testing, formerly used to localize the lesion before the advent of modern imaging, now is useful to establish the extent of the dysfunction, provide a baseline measurement of cognitive function, and help to optimize rehabilitation posttreatment. The advantages of SPECT, PET, BEAM, and MEG scans over the above diagnostic tests are as yet unclear.
❍ How should therapy be altered if a patient with preexisting psychiatric disease presents with a brain tumor?
Clinicians should be especially aware of drug–drug interactions, drugs that cause delirium, and those that cause seizures, because patients with cranial neoplasms become more sensitive to all three. Drug dosages should be decreased (use 1–5 mg of haloperidol, for example, instead of 10–20 mg) and serum levels should be monitored. To decrease the risk of delirium, it is better to substitute haloperidol, carbamazepine, valproate, or benzodiazepines for lithium. Likewise, SSRIs, MAOIs, or secondary amines are better tolerated than TCAs, high-potency neuroleptics are safer than low-potency, and the antiparkinsonian agents amantadine or diphenhydramine much less likely to cause anticholinergic delirium than benztropine, trihexyphenidyl, or orphenadrine. Attention should also be paid
to the seizure-causing potential of antipsychotics—haloperidol, molindone, and fluphenazine are somewhat safer than chlorpromazine or clozapine for the control of psychotic symptoms; and lithium, bupropion, and maprotiline are best avoided for mood control for the same reason. Methylphenidate does not lower the seizure threshold and offers the advantage of rapid onset of action. Psychotherapy should be concrete and reality based, involving the family and focusing on education and issues of loss and death. Denial is a useful defense mechanism early in the
course of the illness but becomes maladaptive later on. ECT is contraindicated if there is any evidence of increased intracranial pressure, but a tumor per se is no longer an absolute contraindication.
❍ How should one modify one’s pharmacologic treatment of anxiety disorder in someone with a cranial mass?
Short-acting, low-dose benzodiazepines are much less likely to cause a paradoxical reaction of increased arousal and agitation than longer-acting agents, which also have an increased propensity to cause delirium, especially in older people. Benzodiazepines also raise the seizure threshold. Buspirone does not cause paradoxical reactions or delirium; its only disadvantage being delayed onset and weak effects. Panic attacks from temporal lobe tumors may respond to carbamazepine, valproic acid, and primidone as well as more conventional antidepressants and anxiolytics.
❍ What are the characteristics of a seizure?
Impairment of consciousness (if complex), involuntary movement, behavioral changes, or altered perceptual experiences.
❍ What is temporal lobe epilepsy?
Although the term no longer officially exists, it is still used clinically to describe seizures that are associated with
sensory hallucinations (particularly olfactory), flashbacks, d´ej`a vu or jamais vu, complex verbalizations, automatisms, and autonomic symptoms such as piloerection and nausea. Rarely, TLE can present with cataplexy or catatonia.
❍ How can TLE be differentiated from complex partial or petit mal seizures?
TLE may be either complex or simple. The term “complex partial seizure” is restricted to patients with focal firing combined with an altered level of consciousness; automatisms alone do not make a complex partial seizure.
Petit mal or absence seizures tend to be shorter in length without automatisms or postictal features, unlike TLE.
❍ What characteristics can help confirm the diagnosis of temporal lobe epilepsy?
Subjective alterations, postictal confusion, impaired memory of event, postictal depression, other episodes of nearly identical behavior, and observer confirmation of characteristic automatisms.
❍ Is there any relation between TLE and psychiatric pathology?
The incidence of psychiatric problems is four to seven times greater in those with TLE than in those without.
❍ What psychiatric issues confront patients with epilepsy?
Epileptic patients daily confront the fear of performing normal social activities (such as dating, during adolescence), because their interpersonal relations typically suffer if a seizure is witnessed. American culture stigmatizes epileptics
as an inferior minority group, with consequent negative effect on the self-esteem of those affected by it. Restrictions on activity (operating machinery, driving, swimming, etc.) can be burdensome, and epileptics suffer guilt and possible legal consequences when they ignore these restrictions. As a result of this, family relationships can evolve into abnormal patterns of isolation or dependency.
❍ What patterns of psychopathology are common in those with a seizure disorder?
There are three patterns of psychopathology associated with seizure disorders, but they are poorly characterized and overlap. The first pattern is characterized by perceptual changes, alterations in consciousness, and poor memory of events. The second is more chronic, associated with paranoia, simple auditory hallucinations, and perceptual changes. The third is characterized by persistent depersonalization and/or visual distortions.