Hypothetical Parkinson’s Disease Case Study

Eric Stephen Ekong

UB No: 09026191

04/03/2011

Study submitted as part of the summative assessment in Control Systems 2

Word count: 990

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 Early-Onset Parkinson’s Disease Case Study
Introduction
G.T.H., a 37-year-old Japanese male presented with a mild tremor in upper extremities (especially
fingers of the left hand), high fatigability and feeling of weakness in the upper limbs. When interviewed,
the patient revealed that the symptoms have been persisting for the last 3 months and worsen when he
is under mental or physical stress (the latter relating to general state of health). The patient has an
unremarkable medical history however, recent and lassitude, irritability and persistent constipation
have been also noted. The patients brother was diagnosed with juvenile Parkinson’s disease (PD) at the
age of 19.

Examination and Tests

Uppon physical examination the upper limbs did not present with any weakness. The hands presented
with tremors with fists were rapidly clenched and unclenched, very mild resting tremor was also noted.
Bradykinesia was identified when the patient was required to rapidly tap his fingers against the thumb.
Spontanious dorsiflexion of the great toe occurred during the physical. Significantly, a reduced
frequency in speech was observed. Micrographia was noted when comparing the patient’s current
signature with one from 2 years prior. All of the above are consistent with the initial presentation of PD
[CITATION Ste1 \l 2057 ] however, no marked gait abnormalities were noted.

Genetic testing of a blood sample revealed the presence of the PARK2 gene but the PARK8 gene was
absent. [CITATION Ste1 \l 2057 ]

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Diagnosis
Early-onset PD was the most probable diagnosis however a variety of conditions could have been
causing the symptoms (see Table 1).

Possible Diagnosis Differentiating feature

Multiple system atrophy Relative absence of tremor, early gait instability and
dysphagia
Drug-induced parkinsonism Lack of resting tremor and asymmetry; requires
exposure to dopamine-blocking drugs.
Essential tremor Tremor is the only sign; no response to PD treatment.
Corticobasal degeneration Limb apraxia, sensory abnormalities and early
dementia.
Table 1. This table present the differential diagnosis of PD, detaling the most commonly misdiagnosed associated
conditions. Other alternatives include: Wilson’s disease, Huntington’s disease, progressive supranuclear palsy, familial
prion disease, Lewy body dementia and Alzheimer’s disease. [ CITATION MOV \l 2057 ] [ CITATION Pan \l 2057
]
The diagnosis of PD can only be confirmed via the presence of predominant features of the condition.
[ CITATION Pan \l 2057 ] Tremor and bradykinesia (two major signs) were presented by the patient
however, the patient lacked rigidity in limbs and core. [ CITATION Pan \l 2057 ][ CITATION Sch \l 2057 ]
The slow progression on the symptoms [CITATION Ste1 \l 2057 ] [ CITATION Bri \l 2057 ] and their low
intensity grant credibility to a diagnosis of PD. This is also supported by the asymmetrical effect on the
limbs. [ CITATION Pan \l 2057 ] [ CITATION Sch \l 2057 ] Early-onset PD is rare however, it affects male
more frequently [CITATION Ste1 \l 2057 ][ CITATION Pan \l 2057 ] and 15-20 percent of patients have a
familial history of the condition. [CITATION Ste1 \l 2057 ] [ CITATION Bri \l 2057 ] Early-onset PD (EOPD)
can also have psychological implication at early stages explaining the patient’s altered mental status.
[ CITATION Bri \l 2057 ] [ CITATION MOV \l 2057 ]

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Initial Treatment
Levodopa, an dopaminergic agent, is the most potent treatment for at all stages of PD treatment
[ CITATION Sch \l 2057 ] however, as EOPD patients are expected to require treatment for up to 50 years
[ CITATION Placeholder1 \l 2057 ] the treatment is delayed and symptoms are managed with other
agents to prevent long term complications. [ CITATION Ari \l 2057 ] Eventually all patients will require
levodopa treatment for symptomatic relief. [ CITATION MOV \l 2057 ]

At the early stages, monoamine oxidase (MAO-B) treatment is recommended [ CITATION Sch \l 2057 ] to
remedy the dopamine related symptoms of PD (e.g. tremor or bradykinesia) by inhibiting the
breakdown of dopamine in the nigrostriatal system of the brain. Agents like selegline and rasagline have
been proven to delay the need for levodopa application by 13 months in EOPD. [CITATION Ste2 \l 2057 ]
Whilst selegline has no effect on PD progression, a placebo- controlled study of latter agent indicated a
decrease in deterioration rate [CITATION Ste2 \l 2057 ] [ CITATION Sch \l 2057 ]; this is further indicates
that rasagline decreases the incidence of severe dyskinesia (a severe complication) when contrasted
against Levodopa. [ CITATION Hau \l 2057 ] [ CITATION MOV \l 2057 ]

Alternatively, dopamine agonists (DA-A) (e.g. pramipexole or ropinirole) could be used to initiate patient
treatment; these agents work by promoting the dopaminergic action at the receptor sites. DA-As are
debatably more effective at symptomatic relief than MAO-Bs [ CITATION Sch \l 2057 ] however, they are
much less effective at delaying levodopa application. [CITATION Ste2 \l 2057 ] Additionally these agents
have marked psychological effects namely gambling and stereotypy. (4)

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Prognosis
As PD is a degenerative condition all symptoms will become more pronounced additionally, the patient
will develop rigidity in all limbs. [CITATION Ste1 \l 2057 ] EOPD has a worse outlook than late- onset PD
as 70% of patients develop severe motor complications 3 years post- diagnosis. [ CITATION Sch \l 2057 ]
These include: freezing, motor fluctuations, dyskinesia and falls. [ CITATION MOV \l 2057 ] Complications
like dysautonomia, dementia, non- fluctuating or fixed dystonia are less likely; the latter two may
require surgery. [CITATION Ste1 \l 2057 ] [CITATION Ste2 \l 2057 ]

Symptoms will require levodopa management [ CITATION MOV \l 2057 ] however, if refraction develops
neurosurgical are applied in the late stages of the disease. [ CITATION MOV \l 2057 ] Ventrolateral
thalamotomy and Pallidotomy are used to treat severe tremors, dyskinesia and intermittent dystonia
that do not react to levodopa. [ CITATION MOV \l 2057 ] [ CITATION Ari \l 2057 ] Deep brain stimulation
applied to the thalamus and pallidal regions are used to treat tremors, rigidity and akinesia and reduce
the patients dependency on levodopa. [ CITATION Sch \l 2057 ] [ CITATION Ari \l 2057 ] However, these
treatments are often too expensive and require repeated procedures. [ CITATION Sch \l 2057 ]

Experimental procedures like the application of stem cells or the use of growth factor on nigal cells have
been receiving conflicting reports and therefore are years away from full clinical deployment. [ CITATION
MOV \l 2057 ] [ CITATION Ari \l 2057 ] Various programmes have been developed to alleviate
complications PD patients experience with speech and swallowing. [ CITATION MOV \l 2057 ]

Consultations with a psychiatrist will be necessary as EOPD patients are likely to develop depression and
psychosis. [CITATION Placeholder1 \l 2057 ] It is possible that the above are due to the long term
application of levodopa however, it might part of PD aetiology; additionally, as it will present with
similar signs as PD. [ CITATION Pål \l 2057 ] This patient may develop dysphagia, urinary tract retention,
impotence, hypertension and insomnia [CITATION Ste2 \l 2057 ] therefore potential drug interactions
need to be managed.Visual and auditory hallucination may develop in PD patients as they finally
progress into dementia. [ CITATION Pan \l 2057 ]

Discussion
Parkinson’s is the second most common incurable neurodegenerative condition [ CITATION Sch1 \l
2057 ] that causes an array of motor and non- motor complications. It is often associated in PARK2 gene
mutations, especially in the YOPD form. [ CITATION Bri \l 2057 ] It usually causes a pathology in the
nigral region which usually progresses into Lewy bodies. [ CITATION Pan \l 2057 ] It has been proven
that when treating EOPD targettig the most debilitating signs greatly improves the patients perception
of the condition and can alleviate depression. [CITATION Ste2 \l 2057 ]

More research is required into surgical treatments of the condition as well as the long term effects of
DA-A treatments and their effect in altering the progression of PD. [CITATION Ste2 \l 2057 ]

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References
1. Gancher ST. Parkinson Disease in Young Adults. Oregon Health Sciences University. 2011.

2. Pankratz. Parkinson Disease Overview. Indiana University School of Medicine. 2004

3. Schüpbach. Neurosurgery at an earlier stage of Parkinson disease.

4. Brice. Parkin Type of Juvenile Parkinson Disease.

5. MOVE, WE. Parkinson's Disease. [Online]

6. Gancher, Stephen T. Parkinson Disease in Young Adults: Treatment & Medication.

7. Surgical Treatment of Parkinson Disease. Arif I Dalvi, MD.

8. Parkinson Disease in Young Adults: Treatment & Medication. Gancher, Stephen T.

9. Ten-year follow-up of Parkinson's disease patients randomized to initial therapy with ropinirole or
levodopa. Hauser.

10. Depressive illness in Parkinson’s disease – indication of a more advanced and widespread
neurodegenerative process? Pålhagen.

11. Neurobiology and treatment of PD. Schapira.

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