Haldol/Haloperidol - Clinical Medication Sheet


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Haldol/Haloperidol - Clinical Medication Sheet
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Haldol/Haloperidol - Clinical Medication Sheet
From:   Nurses - Clinical Medication Sheet: Haldol/Haloperidol

Blocks postsynaptic dopamine receptors in the brain

Contraindications                           Side Effects

CNS depression                               Rash
Coma                                               Blurred vision
Parkinsonism                                   Tardive dyskinesia
                                                       Neuroleptic malignant syndrome
                                                       Severe extrapyramidal reactions

Advise patient  to avoid alcohol while taking this drug.
Do not withdraw drug abruptly unless required by severe adverse reactions.
Drowsiness and dizziness usually subside after a few weeks.
Dry mouth may be relieved with hard candy or gum.
Warn patient  to avoid activities that require alertness or psychomotor
coordination until CNS effects of the drug are known.


HD patients, like others with injuries to the brain, are highly vulnerable
to side effects, cognitive side effects, of medications. The physician should
begin with low doses and advance medicines slowly.

Polypharmacy should be avoided where possible. Many of the drugs used in treating symptoms of HD, such as neuroleptics and antidepressants, will not have immediate efficacy and patients need to be told that they may feel worse before they feel better, because they will experience the side effects, before the beneficial effects have appeared.

Three classes of medication are commonly used to suppress chorea in
Huntington's disease: neuroleptics, such as haloperidol and fluphenazine;
benzodiazepines, such as clonazepam and diazepam;  and dopamine depleting agents, such as reserpine and tetrabenazine.   Each class has its advantages and disadvantages.

The suppression of movement, regarded as a side effect when neuroleptics are used to treat psychosis,  is the desired effect when they are used to treat chorea. Therefore the most popular neuroleptic agents are the high potency drugs, which can also induce the most parkinsonism.

Haloperidol and fluphenazine  are most commonly prescribed. They should be started at a low dose, 0.5 to l mg once or twice a day, and  gradually increased to efficacy. Doses higher than 6-8mg per day have not generally been found helpful in treating chorea.

Patients starting neuroleptics should be warned about two unlikely, but
potentially serious adverse effects.  The first is tardive dyskinesia, a syndrome of involuntary movements often first noted in the face and mouth, that develops in some patients taking neuroleptics. Tardive dyskinesia is of concern because the symptoms are usually permanent, and will likely be hard to recognize in someone with HD.

The other serious problem is neuroleptic malignant syndrome, a rare, but
life threatening reaction characterized  by acute onset of delirium, rigidity, and fever, often accompanied by leukocytocis, and elevated CPK.   Families should know about this so that the patient can be given prompt medical attention if it develops.

Among the older neuroleptics, high potency agents such as haloperidol
(Haldol) or fluphenazine (Prolixin) tend to be less sedating, but cause more parkinsonism.
Lower potency agents such as thioridazine (Mellaril) may aid with overactivity and sleeplessness, but tend to be constipating and can cause orthostasis


9/4/97   Dr. Dubinsky wrote: Haloperidol is a non-selective dopamine
receptor blocker and can be used safely with sertraline and lorazepam. Decisions about medications are best made between a clinician who is experienced in the treatment of HD and a well informed patient and their well informed family.  While there are texts and scientific papers about the treatment of the symptoms of HD, they are not written on stone.
October 1997 a readers response:
"Contraindications- Comatose states and CNS depression due to alcohol or other depressant drugs; severe depressive states; previous spastic diseases; lesions of the basal ganglia; Parkinson's syndrome, except in the case of dyskinesias due to levodopa treatment; sensitivity to haloperidol; senile patients with pre-existing Parkinson-like symptoms."

Lesions of the basal ganglia are common in HD.
Contraindications indicate when NOT to prescribe that particular
medication.   To the list of CNS effects reported to be associated with
haloperidol/haldol, we can add Tardive  Dystonia.

Tardive Dystonia is characterized by delayed onset of choreic or dystonic
movements, is often persistent, and has the potential of becoming irreversible.

In other words, it can establish a source or cause of choreic movements
(manifested later) in addition to HD being a source of choreic movements.

The caudate nucleus is part of the basal ganglia.   Lesions of the basal
ganglia are not just common in HD, they are essential to a final diagnosis of symptomatic HD.  If an autopsy is performed on someone whom everyone is positive died from a complication of advanced HD, and no lesions of the basal ganglia are found at least prior to the days of verification of the HD gene the doctors would conclude it might have been something similar to HD but it was other than HD.

Haloperidol/haldol is contraindicated for use with people who have lesions
of the basal ganglia which, by definition, are people who have symptomatic HD.

Excerpts from RxMed
a peer-reviewed website for primary care physicians
(parentheses are writers):

Haloperidol (or, generically, Haldol) is a butyropherone derivative with
antipsychotic properties that has been considered particularly effective in the management of hyperactivity, agitation, and mania.  Haloperidol is an effective neuroleptic and also possesses antiemetic properties; it has a marked tendency to provoke extrapyramidal effects.  (extrapyramidal effects = abnormal involuntary muscle movements)

Comatose states and CNS depression due to alcohol or other depressant
drugs; severe depressive states; previous spastic diseases; lesions of the basal ganglia; Parkinson's syndrome, except in the case of dyskinesias due to levodopa treatment; sensitivity to haloperidol; senile patients with pre-existing Parkinson-like symptoms.   (As another contraindication, one might add HD and also senile patients with pre-existing HD-like symptoms.)

Warnings: Tardive Dyskinesia
Tardive dyskinesia is known to occur in patients treated with neuroleptics
with antipsychotic properties and other drugs with  substantial neuroleptic activity.
Although the dyskinetic syndrome may remit partially or completely if the medication is withdrawn, it is irreversible in some patients.  Since there is a significant prevalence in this syndrome associated with the use of neuroleptic drugs, and since there is no known treatment, chronic use of  these drugs should generally be restricted to patients for whom neuroleptics are known to be effective and for whom there is no alternative therapy available with better risk acceptability.

Tardive dyskinesia
is a syndrome involving dysfunctional, involuntary movements associated with long-term, chronic use of neuroleptic medications, such as Haldol, Prolixin, and Thorazine. These drugs lead to apparent general calming or sedative effect on the individual and are considered major tranquilizers.

Tardive dyskinesia may appear anywhere from three months to several years after initial use of these medications, and withdrawal from neuroleptics often exacerbates the symptoms.

Common tardive dyskinesia movements include, but are not limited to:
facial tics, grimacing, eye blinking, lip smacking, tongue thrusting,
moving one's head back or to the side, foot tapping, ankle movements, shuffled gait, and head nodding.
Tardive dyskinesia may lead to very serious problems, such as
respiratory interference, inability to eat, oral ulcerations, and difficulty

Tardive dyskinesia movements may be confused with stereotypy because of the repetitive nature of both behaviors.

Stereotypy refers to ritualistic, often complex behaviors, such as body and
head rocking, hand-flapping, and complex hand movement patterns. Stereotypy appears to be under voluntary control. In contrast, dyskinesia movements are less complex, less ritualistic, and are not volitional.

Long-term use of neuroleptics is ideal for controlling psychotic symptoms,
but it produces adverse effects some patients. The most notable of these is tardive dyskinesia (TD), a potentially serious side effect. TD is a syndrome of abnormal involuntary movements of the face, tongue, limbs and trunk.

Since there is no proven way to prevent TD in patients who need long term treatment with neuroleptics, the best strategy is to restrict these drugs to well-defined indications, use them in the lowest effective doses, and assess patients at frequent intervals for early signs of TD.

An estimated one-fourth of all patients treated long-term with neuroleptics
have it. A number of have associated an increased risk of TD with older age. In a current study, we found that the incidence of TD within a year of starting neuroleptic treatment was approximately 26 percent among patients aged 45 to 90, compared to the reported incidence of 4 to 5 percent among younger patients.

Time is a critical factor in the course of TD, with most studies reporting
that the symptoms improve gradually or stabilize over a period of years rather than within the first year of follow-up. This finding supports the view of TD as a syndrome that follows a continuum from resolved to persistent, rather than being either a reversible or irreversible condition.

Severe complications
While TD is usually mild, it can produce physical and psychosocial
Severe oral dyskinesia may result in dental and denture problems that can progress to ulceration and infection of the mouth, as well as unintelligible speech.
Gait disturbances due to limb dyskinesia may leave patients vulnerable to falls and injuries.