All neuroleptics impact upon the brain. This results in many organs of the body becoming dysfunctional. CARDIAC DEATH
Sudden risk of cardiac death (Straus et al 2004)
Atypicals and Typicals caused sudden cardiac death rate compared with non neuroleptic patients (Kuehn 2009)
CONSTIPATION/ BOWEL OBSTRUCTION (Dome et al 2007)
(Hibbard et al 2009)
Physiology:
Intestine muscles have slower contractions
Direct peripheral anticholinergic side effect
DECREASED BASAL METABOLIC RATE (BMR)
Resulting
from T 4 deficiency. Erasmus, U. (1986,1993), Kutsky (1973)
DEATH
Sudden deaths of patients
who were medicated with high dosages of neuroleptics -. Reports are
available from Simpson et al (1987), Mehtonen et al (1991) and Thompson.
(1994).
UK, there were thirteen
sudden deaths of patients who were medicated with Pimozide.
Thomas (1997) refers to
the death of Orville Blackwood in 1991 from heart failure, which resulted
from being injected with a cocktail of Promazine and Fluphenazine.
Whitaker (2002): reports
20 people died whilst taking Olanzapine out of 2,500.
EXTRA
PYRAMIDAL SYSTEM IN THE BRAIN
This
system is implicated by neuroleptics and pertain particularly to abnormal body movements. They include: Extra Pyramidal Side
Effects, Tardive Dyskinesia, Tardive Dystonia and
Akathesia - the latter is included in the psychological side effects section as
the emotions are highly negativelyimplicated. All three iatrogenic conditions are thought to stem from the brains dopamine nigrostriatal pathway due to the blocking of dopamine by
neuroleptics.
1. Extra pyramidal side effects (E.P.S.)
Discovered in 1954, these side
effects result from the neuroleptic prescribing
- the patient displays Parkinsonion symptoms.
Fine body tremor, which
ranges from being almost imperceptible to incessant shaking.
Bradykinesia - the
slowing down of large muscle movement so that the patient appears stupid
and/or clumsy.
Unresponsive to everyday
situations going on around them.
Flat, vacant expression.
Zombie appearance
Excessive salivation
EPS are more prominent
with typical neuroleptics
To
combat the EPS side effects, anti-cholinergic drug,which are also prescribed for Parkinson's disease, have their own side effects.
1a Anticholinergic Side Effects
A. Within the Peripheral Nervous System (Leiberman 2004)
Blurred
vision
Headaches
Dry eyes
Dry mouth
Increased heart rate
Difficulty
in urinating
Constipation
B. Within the Central Nervous System (Lieberman 2004)
Impaired Concentration
Confusion
Attention deficit
Memory impairment
Several studies have indicated that long-term neuroleptic
use is associated with cognitive deterioration and atrophy of the
brain. Chronic use of neuroleptics precedes Parkinson's disease.
2. TARDIVE DYSKINESIA (TD)
Grossly disfiguring and include:
The lower jaw moves in
sideways movement.
The lips become pursed with
the patient sucking and smacking of the lips.
Blowing in and out of the
cheeks.
Facial grimacing.
Abnormal tongue movements
i.e. the tongue quivers - protrudes
Finger movements as though
an invisible guitar is played.
Body actions are
involuntary, potentially irreversible and there is no proven treatment
1959 TD first reported
with link to neuroleptics – TD
TD = damage to brain
neurons – long term causes nerve degeneration
TD risk increases from
chronic long-term exposure Klawans (1973), Smith et al. (1978) and
Mukherjee et al (1982).
TD can appear within 6
months
TD caused by both typical
and atypical drugs
TD is masked by atypicals
but re-emerges after neuroleptic cessation.
Neuroleptic means the
neurone is literally 'seized’
90% of patients diagnosed
with TD resulting from typical neuroleptics. Crane, (1968).
Supplements which help
elimination of free radicals, which causes brain damage
Vitamin E
Eye Q
Tardive
Dyskinesia causes damage to the brain tissue:
Neuroleptics and Brain
Damage: An Annotated Bibliography
Los Angeles Times January 15, 2009 Thomas H. Maugh II
"Zyprexa, Risperdal and Seroquel, among the 10 most commonly
prescribed medications, are just as likely as older antipsychotic drugs to cause
a fatal heart attack, a study finds".
HYPOTHERMIA /HYPERTHERMIA
Likely cause:
TSH deficiency
Body temperature
unregulation
Resulting from disrupted
and lowered BMR. Erasmus (1986,1993)
Unawareness of body
temperature
Hypothermia or
hyperthermia can occur.
Death from heat stroke
Due to an Anticholinergic side effect - reduced sweating
HYPOTHERMIA (Blass et al, 2004)
INCREASED SUN SENSITIVITY
KIDNEY DAMAGE
Condition more prone when polypharmacy is practised
The Merk Manuals ONLINE MEDICAL MANUALS
May result from NMS
Damaged muscles release the protein myoglobin (myoglobinuria)
Toxic to kidneys
Urine turns brown
LIVER DAMAGE
(Oscanli et al 2006)
Jaundice (yellowing of skin) may indicate liver damage
METABOLIC SYNDROME
This life threatening syndrome includes obesity, type 2
diabetes mellitus, hyperlipidaemia (high cholesterol) and diabetic ketoacidosis
(Lieberman 2004, Usher et al 2006), abdominal obesity, insulin resistance and
hypertension. A study by Heiskanen et al (2003) shows that metabolic syndrome with atypical and
typical neuroleptics was2-4 times
higher than people who are not prescribed neuroleptics.
1. Obesity - Endocrine Effect
ACTH deficiency Kutsky,
(1973)
Dysregulation of
cortisol causes excessive abdominal fat
Decreased Thyroxine (T4) causes reduction in BMR slowing down the burning of body
fat @ cholesterol for energy
Shrinkage of adrenal glands creates decreased ability to use body fat for energy.
Increased appetite
2. Diabetes
Excessive thirst is one symptom
Cortisol imbalance - hyperglycaemia
Increasing insulin resistance (Pao et al 2007)
Duke University issued a
report (2002) identifying:
289 cases of diabetes in
patients who had been prescribed Olanzapine. These researchers stated:
"Of the 289 cases of diabetes linked to the use of Olanzapine, 225
were newly diagnosed cases. 100 patients developed ketosis (a serious
complication of diabetes). 22 patients developed pancreatitis –
potentially life-threatening condition. 23 deaths, including that of a
15-year-old adolescent who died of necrotising pancreatitis, a condition
where the pancreas breaks down and dies. 71 % occurred within six months
of starting the drug and many cases were associated with moderate weight
gain."
1994 Duke University
team first reported a diabetes link with Clozapine.
2001 384 reports of
diabetes were associated with Clozapine.
NASAL CONGESTION
Direct noradrenergic side effect
NEUROLEPTIC MALIGNANT SYNDROME (NMS) Dysregulated sympathetic nervous system hyperactivity is responsible for NMS
(Gurrera 1990).
This is a potentially fatal condition of neuroleptic prescribing and can be
associated with rapid and large increases in neuroleptic dose and also in
conjunction withother
neuroleptics (polypharmacy). Occurs in 3% of people with a predominance towards men. Mortality rates for NMS
6%. (Benzer 2002); 30% mortality rate (The Merk Manuals)
Clinical symptoms include:
Hyperpyrexia
Altered mental status
Hypertension
Hypotension
Tachycardia
Tremor
Incontinence Muscarinic Sign
Generalised muscle rigidity Muscarinic Sign
Sweating Muscarinic Sign
Seizures
Cardiac dysarrythmia
Kidney failure
Respiratory failure Muscarinic Sign
Sialorrhea (drooling) Muscarinic Sign
Dysarthria (difficulty in
speaking) Muscarinic Sign
Elevated creatinine
phosphokinase (CPK) enzymes. Caused by muscle & skeletal breakdown. Known as rhabdomyolysis.
Elevated white blood cells
All neuroleptics (typical and
atypical) may precipitate NMS.
Potent neuroleptics eg,
Haloperidol, Fluphenazine, Modecate, Prochlorperazine, (Compazine),
Promethazine (Phenergan), Clozapine (Clozaril), Risperidone (Risperdal,
are associated with NMS.
OSTEOPOROSIS
Calcitonin deficiency
Bone thinning (Meaney, A.M., et al 2004)
Bone loss of
strength
Bone pain
Fractures
Osteoporosis has also been
connected with hyperprolactemia and a vulnerability to hip fractures.
Neurolepticed males have been found to have reduced bone density (Hummer et al
2005) and therefore have the potential for osteoporosis. Increased levels of
cortisol (Annals of Internal Medicine 2005) was found in patients with
osteoporosis and may possibly be the cause of neuroleptic induced
osteoporosis.
Females have been found to have loss of bone mass. (Purificación
Rey-Sánchez 2009)