Task 7: Neuropsychiatry
General __________________________________________________________________________
Kolb, B. & Whishaw, I.Q. (2015). Fundamentals of Human Neuropsychology (7th Edition)
27.7: motor disorders
The group of diseases comprising motor disorders has clinical symptoms marked by abnormalities in
movement and posture referable to dysfunctions of the basal ganglia. Although the most obvious
symptom is the motor affliction, all produce cognitive changes as well, changes that become
especially marked as motor disorders progress.
Clinically, two groups of motor symptoms are distinguished:
1. Loss of movement, referred to as a hypokinetic-rigid syndrome (Parkinson’s disease)
2. Increased motor activity, known as a hyperkinetic-dystonic syndrome (Tourette’s
syndrome).
9.2: The brainstem: Motor control (p.246)
Two different—in many ways opposite—kinds of movement disorders result from basal ganglia
damage, depending on the injury.
If cells of the caudate putamen are damaged, unwanted
choreiform (writhing and twitching) movements called
dyskinesias may result. Such involuntary movements, or
hyperkinetic symptoms (involuntary movements) appear as
unwanted tics and vocalizations peculiar to Tourette’s
syndrome.
o caudate putamen damage
If the cells of the basal ganglia are left intact but its inputs are
damaged, the injury results in difficulty making movements—
that is, in hypokinetic symptoms. Parkinson’s disease, caused
by the loss of dopamine cells from the substantia nigra and of
their input into the basal ganglia via the nigrostriatal pathway,
is characterized by muscular rigidity and difficulty initiating and
performing movements.
o Inputs of the basal ganglia are damaged
PART 1: Parkinson disease_____________________________________________________________
Kolb, B. & Whishaw, I.Q. (2015). Fundamentals of Human Neuropsychology (7th Edition)
27.7: motor disorders
Parkinson’s disease is a hypokinetic disorder and s fairly common.
Incidence estimates vary from 0.1 - 1 % of the population worldwide, and the incidence rises
sharply in old age. Among about 10 million patients with Parkinson’s worldwide, incidence is
higher in countries with longer life expectancies.
The four major symptoms of Parkinson’s disease are tremor, muscular rigidity, involuntary
movement, and postural disturbance; each symptom may be manifested in different body
parts in different combinations.
Because some symptoms reflect the acquisition of abnormal behaviours (positive symptoms)
and others the loss of normal behaviours (negative symptoms), we consider Parkinson’s
symptoms within these two major categories.
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,Positive symptoms (abnormal behaviours) – common in Parkinson’s disease. They are inhibited in
healthy people but released from inhibition in the process of the disease.
Tremor at rest - Alternating movements of the limbs when they are at rest stop during
voluntary movements or during sleep.
o Hand tremors often have a “pill-rolling” quality, as if a pill were being rolled between
the thumb and forefinger.
Muscular rigidity - Movement is resisted, but with sufficient force the muscles yield for a
short distance and then resist movement again. Thus, complete passive flexion or extension
of a joint (gewricht) occurs in a series of steps, giving rise to the term cogwheel rigidity.
Involuntary movements - These may consist of continual changes in posture, sometimes to
relieve tremor and sometimes to relieve stiffness, but often for no apparent reason. These
small movements or posture changes, sometimes referred to as akathesia or cruel
restlessness, may be concurrent with general inactivity. Other involuntary movements are
distortions of posture, such as those during oculogyric crisis (involuntary turns of the head
and eyes to one side), which last for periods of minutes to hours.
Negative symptoms (loss of normal behaviours) – patients severely affected with Parkinson are
divided into 5 groups, those with:
Postural disorders
o A disorder of fixation consists of an inability to maintain or difficulty in maintaining a
body part in its normal position in relation to other body parts. Thus, a person’s head
may droop forward or a standing person may gradually bend forward until he or she
ends up on the knees.
o Disorders of equilibrium consist of difficulties in standing/ sitting unsupported. In
less-severe cases, patients may have difficulty standing on one leg, or if pushed
lightly on the shoulders, they may fall passively without taking corrective steps or
attempting to catch themselves.
Righting disorders - Patients have difficulty standing from a supine position (acherover
liggende positie) . Many patients with advanced disease have difficulty even in rolling over,
which is problematic in bed.
Locomotive disorders - Normal locomotion requires supporting the body against gravity,
stepping, balancing while body weight is transferred from one limb to another, and pushing
forward. Patients with Parkinson’s disease have difficulty initiating stepping. When they do
walk, they shuffle with short footsteps on a fairly wide base of support because they have
trouble maintaining equilibrium when shifting weight from one limb to the other.
o Often, patients who have begun to walk demonstrate festination: they take faster
and faster steps and end up running forward.
Speech disturbances - almost complete absence of tone (prosody) in the speaker’s voice.
Akinesia - A poverty or slowness of movement may also manifest itself in a blank facial
expression or lack of blinking, swinging the arms when walking, spontaneous speech, or
typical fidgeting movements. Akinesia also manifests in difficulty making repetitive
movements, such as tapping, even in the absence of rigidity. People who sit motionless for
hours demonstrate akinesia in its most striking manifestation.
Genetic risk factors for Parkinson’s Disease
Most Parkinson’s cases are not likely inherited, but about 25 percent of people with Parkinson’s do
have a living relative with the disease. Researchers and research organizations analyzed over 13,000
Parkinson’s cases and nearly 100,000 controls, all of European ancestry, and identified more than
two dozen genome-wide variations the more variants a person has, the greater the risk of
developing the disease.
Progression of Parkinsonism
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, Positive and negative symptoms of Parkinson’s disease begin insidiously, often with a tremor in one
hand and slight stiffness in the distal parts of the limbs. The disease is progressive, but the rate at
which symptoms worsen is variable. Usually 10 to 20 years elapse before symptoms cause incapacity.
A most curious aspect of Parkinson’s disease is its on-again–off-again quality: symptoms may appear
suddenly and disappear just as suddenly. Partial remission may also occur in response to interesting
or stimulating situations (man who jumped out of his wheelchair to save a drowning man).
Causes of Parkinsonism
The three major types of Parkinson’s disease are idiopathic, postencephalitic, and drug-induced.
Parkinson’s disease may also result from arteriosclerosis (aderverkalking), syphilis, tumor
development, carbon monoxide poisoning, or manganese intoxication.
Idiopathic - the cause of idiopathic Parkinson’s disease is unknown. Its origin may be familial,
or it may be part of the aging process, but it is also widely thought to have a viral origin. The
idiopathic type most often develops in people older than 50 years of age. disease of
getting older.
Postencephalitic - originated in the sleeping sickness (encephalitis lethargica) that appeared
in the winter of 1916–1917 and vanished by 1927. Constantin von Economo (1931)
demonstrated a unique pattern of brain damage—namely, the death of cells in the
substantia nigra. a sleeping disease
o The latency between the initial occurrence of the sleeping sickness and subsequent
occurrences of the disease has never been adequately explained. Specific searches
for viral particles or virus-specific products in Parkinson patients without encephalitis
have revealed no evidence of viral cause, although it is still believed to be likely.
Drug- induced - disease developed most recently and is associated with ingesting various
drugs, particularly major tranquilizers. The symptoms are usually reversible but are difficult
to distinguish from those of the genuine disorder.
External agents - Langston and coworkers (1983, 2008) reported that a contaminant, MPTP,
of synthetic heroin is converted to MPP1, which is extremely toxic to dopamine cells. A
number of young drug users were found to display a complete parkinsonian syndrome
shortly after using contaminated drugs. This finding suggests that other substances might
cause similar effects.
o The results of later demographic studies of patient admission in various cities show
an increased incidence of patients contracting Parkinson’s disease at ages younger
than 40. This finding suggests that water and air might contain environmental toxins
that work in a fashion similar to MPTP.
Dopamine - The cells of the substantia nigra are the point of origin of fibers that extend into
the frontal cortex and basal ganglia and to the spinal cord. The neurotransmitter at the
synapses of these projections is dopamine. It is demonstrated that the amount of dopamine
in the brain is reduced by more than 90 percent and often to undetectable amounts in
Parkinson disease a lack of dopamine or, in drug-induced cases, as a lack of dopamine
action.
o Dopamine depletion may not account for the whole problem in some people,
however, because decreases in norepinephrine have been recorded, and numerous
results show that cells in some basal ganglia nuclei may degenerate as well.
Treating Parkinson’s disease
No known cure for Parkinson’s disease exists, and none will be in sight until the factors that produce
the progressive deterioration of the substantia nigra are known. Thus, treatment is symptomatic
and directed toward support and comfort.
Psychological factors influence the major symptoms of parkinsonism, and a person’s
outcome is strongly affected by how well he or she copes with the disability patients
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