BRAIN DISEASES SUMMARY
PARKINSON’S DISEASE
James Parkinson’s (1817): explained in great detail the clinical characteristics of patients (wrongfully assumed
lesions of the spinal cord).
Parkinson’s disease is a progressive, chronic (no cure) neurological condition. The older you get the higher the
likelihood.
There is no fixed test for diagnosis of Parkinson’s disease, but certain symptoms/severity of symptoms can be
assessed:
- Bradykinesia: rigidity and/or rest tremor.
- Clear response to levodopa
- The onset of the disease is unilateral, also called an asymmetrical disease (does not start at both limbs
at an equal measure).
- Postural instability
- Olfactory loss
Terminology on Parkinson’s disease:
- Parkinson’s disease (PD): idiopathic (we do not know what causes it) parkinsonism
- Parkinsonism: group of disorders with abnormal function of basal ganglia
- Secondary parkinsonism: result of virus, toxins (MPTP for mice causes irreversible parkinsonism),
drugs, tumours
- Vascular parkinsonism: result of multiple small strokes
- Parkinson-plus: mimics PD but with different disorder (MSA, PSP)
PATHOLOGY
Lewy Bodies in neurons of the substantia nigra but also in the cerebral cortex.
There are 6 different stages of Parkinson’s disease (Braak staging) based on clinical symptoms and location of
the Lewy bodies.
,Dopamine levels in Parkinson’s: core feature of Parkinson’s disease is a loss of dopamine. Less dopamine is
produced or present = movement disorder (initiation of movement).
CLINICAL DIAGNOSIS
Bradykinesia = slow movement
- Finger tapping/foot taping
- Handwriting
- Difficulty turning
- Gait
Hypokinesia = less movement
- Facial expression
- Reduced armswing
- Reduced swallowing
TREMOR
Rest tremor (hands): Tremor is around 4 to 6 Hz, and in patients above the age of 70 there is an involvement
of the chin, legs and tongue. Patients diagnosed early, before the age of 40 show an involvement of their legs.
,When patients are walking or doing demanding cognitive tasks they get stressed and the tremor emerges. Re-
emergence of a postural tremor is also called a rest tremor.
Postural tremor:
Freezing: motor complication that can arise at any time of the day, problems with initiation of movement.
(Freezing in revolving doors). Patients develop cues (visual, auditory, sensory) to help with the initiation of
movement.
TREATMENT
Levodopa: After years on medication patients develop motor fluctuations which become more severe with the
progression of the disorder. Over time people become resistant to levodopa. Dyskinesias come in different
forms (jerkiness).
ADVANCED TREATMENTS
The effects of levodopa wear out after long term use, so other advanced treatments are available:
- Apomorphine pump (dopamine agonist): apomorphine injection
- Duodopa pump: a cassette with dopaminergic slush is connected to the intestines
- Deep brain stimulation: electrodes are placed directly into the brain and cause inhibition
, NON-DOPAMINERGIC DOMAINS
Some symptoms of Parkinson’s are not responding to dopaminergic treatment.
1. Cognition
2. Depression
3. Psychotic symptoms
4. Extensive daytime sleepiness
5. Autonomic symptoms
6. PIGD
COGNITION
Cognitive disturbances and dementia: executive functioning, memory, attention and visuospatial components
are all affected. It is crucial to differentiate between what are the symptoms of Parkinson’s and what are side
effects of the drugs.
Risk factors: age, later age of onset, disease duration, severity
PD-MCI: patients should be able to function on their own.
Assessment of cognition: clock drawing, pill questionnaire
Cognitive treatment: Not much to be done. Cholinesterase-inhibitors or Rivastigmine. It can improve cognition
and psychiatric symptoms. However, it results in adverse side effects such as more extreme tremors, nausea
and vomiting (what is the net benefit).
DEPRESSION AND ANXIETY
There is high prevalence of depression and anxiety in Parkinson’s patients. It is challenging to differentiate if
patients are depressed or describe their symptoms realistically, since a lot of questions on the depression
scales overlap with symptoms of Parkinson’s. Loss of initiative and apathy, fatigue and slowness, concentration
and memory problems, insomnia or excessive sleepiness and anorexia or weight loss could all be either
Parkinon’s effects or indication of depression.
Management of depression is done with drug treatment but they should be used with caution as they also
have side effects (balance between benefits and side effects):
- SSRIs: may inhibit dopamine release (recommended to start with them)
- Anticholinergic drugs: may induce cognitive impairment and orthostatic hypertension (increased fall
risk)
DIFFERENTIAL DIAGNOSIS
Cognition is a crucial factor for recognizing Parkinson’s.
PARKINSON’S DISEASE
James Parkinson’s (1817): explained in great detail the clinical characteristics of patients (wrongfully assumed
lesions of the spinal cord).
Parkinson’s disease is a progressive, chronic (no cure) neurological condition. The older you get the higher the
likelihood.
There is no fixed test for diagnosis of Parkinson’s disease, but certain symptoms/severity of symptoms can be
assessed:
- Bradykinesia: rigidity and/or rest tremor.
- Clear response to levodopa
- The onset of the disease is unilateral, also called an asymmetrical disease (does not start at both limbs
at an equal measure).
- Postural instability
- Olfactory loss
Terminology on Parkinson’s disease:
- Parkinson’s disease (PD): idiopathic (we do not know what causes it) parkinsonism
- Parkinsonism: group of disorders with abnormal function of basal ganglia
- Secondary parkinsonism: result of virus, toxins (MPTP for mice causes irreversible parkinsonism),
drugs, tumours
- Vascular parkinsonism: result of multiple small strokes
- Parkinson-plus: mimics PD but with different disorder (MSA, PSP)
PATHOLOGY
Lewy Bodies in neurons of the substantia nigra but also in the cerebral cortex.
There are 6 different stages of Parkinson’s disease (Braak staging) based on clinical symptoms and location of
the Lewy bodies.
,Dopamine levels in Parkinson’s: core feature of Parkinson’s disease is a loss of dopamine. Less dopamine is
produced or present = movement disorder (initiation of movement).
CLINICAL DIAGNOSIS
Bradykinesia = slow movement
- Finger tapping/foot taping
- Handwriting
- Difficulty turning
- Gait
Hypokinesia = less movement
- Facial expression
- Reduced armswing
- Reduced swallowing
TREMOR
Rest tremor (hands): Tremor is around 4 to 6 Hz, and in patients above the age of 70 there is an involvement
of the chin, legs and tongue. Patients diagnosed early, before the age of 40 show an involvement of their legs.
,When patients are walking or doing demanding cognitive tasks they get stressed and the tremor emerges. Re-
emergence of a postural tremor is also called a rest tremor.
Postural tremor:
Freezing: motor complication that can arise at any time of the day, problems with initiation of movement.
(Freezing in revolving doors). Patients develop cues (visual, auditory, sensory) to help with the initiation of
movement.
TREATMENT
Levodopa: After years on medication patients develop motor fluctuations which become more severe with the
progression of the disorder. Over time people become resistant to levodopa. Dyskinesias come in different
forms (jerkiness).
ADVANCED TREATMENTS
The effects of levodopa wear out after long term use, so other advanced treatments are available:
- Apomorphine pump (dopamine agonist): apomorphine injection
- Duodopa pump: a cassette with dopaminergic slush is connected to the intestines
- Deep brain stimulation: electrodes are placed directly into the brain and cause inhibition
, NON-DOPAMINERGIC DOMAINS
Some symptoms of Parkinson’s are not responding to dopaminergic treatment.
1. Cognition
2. Depression
3. Psychotic symptoms
4. Extensive daytime sleepiness
5. Autonomic symptoms
6. PIGD
COGNITION
Cognitive disturbances and dementia: executive functioning, memory, attention and visuospatial components
are all affected. It is crucial to differentiate between what are the symptoms of Parkinson’s and what are side
effects of the drugs.
Risk factors: age, later age of onset, disease duration, severity
PD-MCI: patients should be able to function on their own.
Assessment of cognition: clock drawing, pill questionnaire
Cognitive treatment: Not much to be done. Cholinesterase-inhibitors or Rivastigmine. It can improve cognition
and psychiatric symptoms. However, it results in adverse side effects such as more extreme tremors, nausea
and vomiting (what is the net benefit).
DEPRESSION AND ANXIETY
There is high prevalence of depression and anxiety in Parkinson’s patients. It is challenging to differentiate if
patients are depressed or describe their symptoms realistically, since a lot of questions on the depression
scales overlap with symptoms of Parkinson’s. Loss of initiative and apathy, fatigue and slowness, concentration
and memory problems, insomnia or excessive sleepiness and anorexia or weight loss could all be either
Parkinon’s effects or indication of depression.
Management of depression is done with drug treatment but they should be used with caution as they also
have side effects (balance between benefits and side effects):
- SSRIs: may inhibit dopamine release (recommended to start with them)
- Anticholinergic drugs: may induce cognitive impairment and orthostatic hypertension (increased fall
risk)
DIFFERENTIAL DIAGNOSIS
Cognition is a crucial factor for recognizing Parkinson’s.
