Pre-existing Parkinsons disease or dementia with Lewy bodies

Interactions
Amiodarone: Q-Tc interval prolongation (potentially dangerous change in heart rhythm). Amphetamine and methylphenidate: counteracts increased action of norepinephrine and dopamine in patients with narcolepsy or ADD/ADHD
Epinephrine:  action antagonized, paradoxical decrease in blood pressure may result
Guanethidine:  antihypertensive action antagonized
Levodopa:  decreased action of levodopa
Lithium:  rare cases of the following symptoms have been noted: encephalopathy, early and late extrapyramidal side effects, other neurologic symptoms, and coma. Methyldopa:  increased risk of extrapyramidal side effects and other unwanted central effects
Other central depressants (alcohol, tranquilizers, narcotics):  actions and side effects of these drugs (sedation, respiratory depression) are increased. In particular, the doses of concomitantly used opioids for chronic pain can be reduced by 50%. Other drugs metabolized by the CYP3A4 enzyme system: inducers such as carbamazepine, phenobarbital, and rifampicin decrease plasma levels and inhibitors such as quinidine, buspirone, and fluoxetine increase plasma levels
Tricyclic antidepressants:  metabolism and elimination of tricyclics significantly decreased, increased toxicity noted (anticholinergic and cardiovascular side effects, lowering of seizure threshold)

Discontinuation
The British National Formulary recommends a gradual withdrawal when discontinuing antipsychotics to avoid acute withdrawal syndrome or rapid relapse. Symptoms of withdrawal commonly include nausea, vomiting, and loss of appetite. Other symptoms may include restlessness, increased sweating, and trouble sleeping. Less commonly there may be a feeling of the world spinning, numbness, or muscle pains. Symptoms generally resolve after a short period of time.There is tentative evidence that discontinuation of antipsychotics can result in psychosis.
Given that antagonism of D2 receptors is more beneficial on the positive symptoms of schizophrenia and antagonism of 5-HT2 receptors on the negative symptoms, this characteristic underlies haloperidols greater effect on delusions, hallucinations and other manifestations of psychosis. Haloperidols negligible affinity for histamine H1 receptors and muscarinic M1 acetylcholine receptors yields an antipsychotic with a lower incidence of sedation, weight gain, and orthostatic hypotension though having higher rates of treatment emergent extrapyramidal symptoms. Haloperidol acts on these receptors: (Ki)

D1 (silent antagonist) – Unknown efficiency
D5 (silent antagonist) – Unknown efficiency
D2 (inverse agonist) – 0.7 nM
D3 (inverse agonist) – 0.2 nM
D4 (inverse agonist) – 5–9 nM
σ1 (irreversible inactivation by haloperidol metabolite HPP+) –  3 nM
σ2 (agonist): 54 nM
5HT1A receptor agonist –  1927 nM
5HT2A (silent antagonist) –  53 nM
5HT2C (silent antagonist) – 10,000 nM
5HT6 (silent antagonist) – 3666 nM
5HT7 (irreversible silent antagonist) – 377.2 nM
H1 (silent antagonist) – 1,800 nM
M1 (silent antagonist) – 10,000 nM
α1A (silent antagonist) – 12 nM
α2A (silent antagonist) – 1130 nM
α2B (silent antagonist) – 480 nM
α2C (silent antagonist) – 550 nM
NR1/NR2B subunit containing NMDA receptor (antagonist; ifenprodil site): IC50 – 2,000 nM

Pharmacokinetics
By mouth
The bioavailability of oral haloperidol ranges from 60 to 70%. However, there is a wide variance in reported mean Tmax and T1/2 in different studies, ranging from 1.7 to 6.1 hours and 14.5 to 36.7 hours respectively. Intramuscular injections
The drug is well and rapidly absorbed with a high bioavailability when injected intramuscularly. The Tmax is 20 minutes in healthy individuals and 33.8 minutes in patients with schizophrenia.