Patient 1: This 65 year-old man of a Bantu tribe was admitted because of loss of memory for one year and recent intermittent confusion. There was no significant past medical or family history. On examination there was bradykinesia and cogwheeling of both upper limbs and axial rigidity. Both knees were contracted and thus difficult to examine. The right plantar was upgoing. There were no cerebellar signs. The mental state confirmed cognitive decline. The hemoglobin (Hb) was within normal range. CSF was not taken. A chest X-ray was unremarkable. L-dopa was not given, because it was out of stock. The origin of the patient’s Parkinsonism remained unclear.

Patient 2: This 70 year-old man of a Bantu tribe was admitted because of dysuria and inability to walk for one day. There was no significant past medical or family history. He had bradykinesia, rigidity and cogwheeling of the right upper limb only for the last years. Reflexes were all normal. There were no cerebellar signs or gait disturbances and the mental state was normal. The Hb was 8 g/dL, CSF was not taken. Abdominal ultrasound showed pronounced bilateral hydronephrosis. L-dopa was not given because it was out of stock. According to the UK Parkinson’s Disease Brain Bank criteria the patient had a clear Parkinsonian syndrome with only two supportive features of PD (unilateral onset and progressive disorder). We are unable to comment on the patient’s response to L-dopa. Our diagnosis, therefore, was that of possible PD. The patient died of renal failure within 7 days.

Patient 3: This 32 year-old man of a Bantu tribe was admitted because of gradual onset of shaking of the left part of his body for the last four years. In the past, the patient had been treated for tuberculosis. There was no significant family history. On examination there was Hemiparkinsonism of the left side with pronounced resting tremor, bradykinesia and rigidity of the left upper and lower limb. There was also a third nerve palsy right and seventh nerve upper motor neuron palsy left. The gait was not majorly impaired, there were no cerebellar signs and the mental state was normal. Hb and erythrocyte sedimentation rate (ESR) were within normal range, CSF and chest X-ray were not taken. A CT scan, conducted elsewhere, showed a contrast enhancing mass lesion extending from mid brainstem towards the third ventricle and into the basal ganglia on the right side. The symptoms improved moderately on L-dopa. The diagnosis was that of likely tuberculoma causing Hemiparkinsonism (secondary Parkinsonism). The patient was referred to a university hospital.

Patient 4: This 54 year-old man of a Bantu tribe was admitted because of clumsiness of mainly the right upper limb for two years and vomiting for some days. Past medical history showed a non-insulin dependent diabetes mellitus for 6 years, hypertension, a stroke and a heart attack. There was no significant family history. On examination there was a Parkinsonian facies, bradykinesia and rigidity of all four limbs. Symptoms were most pronounced on the right upper limb, where there was also a resting tremor. There was minimal weakness with increased reflexes on the left side. The patient showed a typical Parkinsonian gait. There were no cerebellar signs. There was foot drop on the right and reduced sensation up to both knees and absent ankle jerks bilaterally. The mental state showed clinical depression. Blood pressure was 190/110 mmHg. Hb was within normal range, random blood glucose was 8 mmol/L. CSF was not taken. The response of Parkinsonian symptoms to L-dopa was good. Referring to the UK Parkinson’s Disease Brain Bank criteria, the patient had a Parkinsonian syndrome and more than three criteria (unilateral onset, resting tremor, progressive disorder, persistent asymmetry of signs and, in particular, good response to L-dopa) supporting a diagnosis of PD. We therefore favored the diagnosis of PD rather than vascular Parkinsonism.

Patient 5: This 52- year old man of the Iraqw tribe was admitted because of clumsiness and shaking of the right upper limb for the last two years. There was no significant past medical or family history. On examination there was a Parkinsonian facies and bradykinesia, rigidity and resting tremor on the right upper limb. There was axial rigidity, but postural reflexes and gait was not impaired. The mental state was unremarkable. No further investigations were performed. All symptoms responded very well to L-dopa. According to the UK Parkinson’s Disease Brain Bank criteria, the patient had a Parkinsonian syndrome and more than three criteria (unilateral onset, resting tremor, progressive disorder and excellent response to L-dopa) supporting a diagnosis of PD.

Patient 6: This 82 year-old man of the Iraqw tribe was admitted because of acute dysuria and clumsiness of his right side for the last three years. There was also intermittent confusion and loss of memory for the same period. The past medical history showed hypertension, alcohol abuse, pulmonary and abdominal tuberculosis. There was no significant family history. On examination, there was a stiff neck and a Parkinsonian facies. There was also a seventh nerve upper motor neuron palsy, possibly due to a previous stroke. Bradykinesia and rigidity were symmetrical in all four limbs, resting tremor was present in both upper limbs. There was a typical Parkinsonian gait, but no cerebellar signs. The mental state showed disorientation to time and place and decline of cognitive function. BP was 150/95 mmHg. Hb, ESR and white blood count were within normal range. CSF was not taken. The chest X-ray showed old signs of Tb. L-dopa was not given, because it was out of stock. The cause of Parkinsonism remained unclear, a vascular cause is possible.

Patient 7: This 70 year-old man of the Iraqw tribe was admitted because of stiffness and shaking of both legs for the last three years. There was a history of hypertension, family history was unremarkable. On examination there was neck stiffness with cogwheeling. There was no weakness, but bradykinesia of all four limbs and increased muscle tone with cogwheeling in the lower limbs. There was no tremor. The masseter reflex was increased and there was a positive pout reflex. All other reflexes were normal and symmetrical with bilateral upgoing plantars. The patient was unable to walk because of the rigidity, there were no cerebellar signs. The mental state was normal. BP was 182/112 mmHg. Hb and ESR were within normal range. CSF was not taken. L-dopa did not lead to a significant improvement. The diagnosis was Parkinsonism most likely due to cerebrovascular disease.

Patient 8: This 75 year-old man of a Bantu tribe was admitted because of loss of memory and mental confusion for four months. The patient admitted to alcohol abuse, family history was unremarkable. On examination there was a slight Parkinsonian facies, cogwheeling and bradykinesia of both upper limbs more pronounced on the left side. There was action tremor on both upper limbs. The mental state confirmed pronounced cognitive impairment. Hb, urea, sodium and potassium were within a normal range. CSF was not taken. L-dopa was not given, because it was out of stock. The patient was treated with thiamine and benzodiazepines. The cause of Parkinsonism remained obscure. The cognitive decline may have the same origin as the Parkinsonian syndrome or may be due to alcohol abuse.