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Annals of Clinical and Medical
Case Reports
Case Report ISSN: 2639-8109 Volume 8
Emergencies in Parkinsonism
Adel Ekladious1*
and Ramana Waran2
1
Faculty of Health and Medical Sciences, University of Western Australia, 35 Stirling Hwy, Crawley, WA, Australia, South East Region-
al Hospital, 4 Virginia Drive, Bega, NSW, Australia
2
University of Wollongong (UOW), School of Medicine, NSW, Australia, Cass Byres ( Medical student) UOW , school of medicine ,
NSW, Australia
*
Corresponding author:
Adel Ekladious,
Faculty of Health and Medical Sciences, University
of Western Australia, 35 Stirling Hwy, Crawley, WA,
Australia, South East Regional Hospital, 4 Virginia
Drive, Bega, NSW, Australia,
E-mail: ekladiou@gmail.com
Received: 29 Jan 2022
Accepted: 07 Feb 2022
Published: 14 Feb 2022
J Short Name: ACMCR
Copyright:
©2022 Adel Ekladious. This is an open access article dis-
tributed under the terms of the Creative Commons Attribu-
tion License, which permits unrestricted use, distribution,
and build upon your work non-commercially.
Citation:
Adel Ekladious, Emergencies in Parkinsonism. Ann Clin
Med Case Rep. 2022; V8(9): 1-3
1. Abstract
Patients with Parkinsonism may present acutely to the ED with
serious and even life-threatening conditions. Although falls are
a common presentation in advanced Parkinsonism, early presen-
tations with falls should alert the clinician that the patient might
have a Parkinson syndrome other than Parkinson’s disease itself,
including autonomic neuropathy causing orthostatic hypotension.
Patients may present with neuroleptic malignant syndrome, acute
psychosis, marked hypokinesis, freezing gait, aspiration pneumo-
nia, dysphagia, serotonin syndrome, dopamine dysregulation syn-
drome and intestinal pseudo-obstruction.An inpatient admission is
necessary for investigation and observation of these patients. We
present a case of a patient who presented with an uncommon side
effect of a common medication used for Parkinsonism.
2. Case Report
A 60-year-old man presented with weakness leading a fall and
subsequent fracture of his left arm. His medical history was signif-
icant for Parkinsonism, diagnosed at the age of 50. He was being
followed-up regularly by a movement disorder specialist every
three months. His medications included levodopa/carbidopa 750
mg daily, rotigotine dermal patch 6 mg daily and amantadine 300
mg daily for one year. He started to develop motor fluctuations of
delayed ‘on’ and unpredictable ‘off’ periods and painful dyskine-
sia. The patient’s partner reveled to his specialist that he had also
started to develop non-motor symptoms of a Rapid Eye Movement
disorder, where the patient started to enact his dreams by punching
his partner. Clonazepam did not improve his symptoms, but mela-
tonin did to moderate effect. The patient started to experience gait
freezing and dyskinesia, so rotigontine was ceased and levodopa/
carbidopa was increased to one gram daily. A MAO inhibitor and
COMT inhibitor were added with no improvement. 18 months ago,
he was started on intermittent apomorphine SC by his specialist
with significant symptomatic improvement. He was subsequent-
ly started on a continuous infusion of apomorphine 4mg/hour 6
months later. His sleep improved significantly. When he presented
to the ED, examination by an Advanced Trainee revealed that the
‘pull-test’ was positive and the patient looked jaundiced and pale.
The remainder of the examination, including the chest, abdomen,
lymph nodes, muscles and joints, were unremarkable. There was
no postural hypotension, no tremor, and no rigidity. The patient
had a chest X-ray and an ECG which showed no abnormal findings
apart from fracture in the left clavicle. An orthopedic Registrar
reviewed the patient and advised for symptomatic management of
Parkinsonism. A movement specialist nurse advised for the patient
to continue on the same medications. In the ED, the Haemoglo-
bin was 7 grams/DI, Haematocrit 19, MCV 95, Platelets 190, AST
30, total bilirubin 4, and unconjugated bilirubin 3. The patient was
given 3 units of packed red cells. Gastroenterology booked the pa-
tient for an upper and lower endoscopy the following day, which
did not show any signs of bleeding. On Day 3 the Senior Registrar
received a call from haematology. They informed the treating team
that the patient had a high LDH, low haptoglobin and spherocy-
tosis on the blood film. Serum electrophoresis did not show clon-
ality. Serum B12, folate and copper were normal. Methylmalonic
acid, homocysteine, zinc levels, immunoglobulin, immunopheno-
typing, the kappa/lambda ratio, flow cytometry, serum nitric oxide,
and G6PD levels were also normal. Haemoglobin electrophoresis
http://acmcasereports.com 1
http://acmcasereports.com 2
Volume 8 Issue 9 -2022 Case Report
showed normal HbA2 and no evidence of thalassemia or sickle
cell anemias. An immune screen, including ANA, ENA, Coombs’
test, Anti-Scl-70, Anti-RPN, rheumatoid factor, complement, an-
ti-CCP, and an anti-synthetase screen were all either negative or
normal. A CT head, neck, chest, abdomen, pelvis, and ultrasound
of the testes were also all normal. The patient was reassured and
sent home with plans for a follow-up with his specialist and the
orthopaedic team as an outpatient. The patient’s specialist advised
for the patient to continue on his medication for Parkinson’s as it
appeared to be working well to control his symptoms. Two weeks
later, the patient presented to the ED after having another fall. The
cause of the fall was unclear. His Haemoglobin had dropped to 5
grams/DI, and the patient had an elevated AST, LDH and uncon-
jugated bilirubin. The haematology registrar was called to look at
the peripheral blood film, and he confirmed that the patient had a
hemolytic anemia. In consultation with his consultant, the regis-
trar advised to send the patient to the haematology department for
consideration of a bone marrow biopsy. The patient’s movement
disorder specialist advised for him to continue taking the same
medication. The patient was reviewed by cardiology who advised
that the patient should continue on telemetry and should arrange
for a transthoracic echocardiogram. Four units of packed red cells
were infused. The patient later had a bone marrow biopsy which
showed normal erythropoiesis. An echocardiogram was performed
which showed normal muscles and valves, and there was normal
cardiac systolic and diastolic function. The patient was eventual-
ly seen by the consultant hematologist who examined the patient
and his blood film diagnosed them with drug-associated bite cell
hemolytic anemias. His medication was reviewed by the pharma-
cist and immunologist, who agreed that the patient had a hemolyt-
ic anemia due to apomorphine. The apomorphine was ceased in
consultation with his specialist. The patient was seen by his neu-
rologist and specialist nurse. In consultation with the patient, it
was decided that the patient was to receive levodopa/carbi-dopa
intestinal infusion gel. The patient had a percutaneous endoscopic
gastrostomy into the jejunum with 2 grams of levodopa and 500
mg carbidopa. Patient complications such as dislodgement of the
jejunal tube, catheter migration, bezoar formation, intestinal ob-
struction, abdominal pain, flatulence and constipation were all ex-
plained to the patient.
The patient was discharged home with plans for outpatient reha-
bilitation and follow-up with a specialist Parkinsonism nurse. 10
months later, the patient attended the ED because he could not feel
his legs and had had a fall. The patient was admitted to an acute
assessment unit. They were seen by neurology, who performed an
EMG and diagnosed the patient to have a peripheral sensory neu-
ropathy.
His blood tests confirmed the patient had a haemolytic anaemia,
however there was no clear cause to explain the haemolysis. The
patient was transfused with 3 units of packed RBC. His serum B12
was 12 (300-600), folate was within normal limits and homocys-
teine and MMA were elevated. A bone marrow biopsy confirmed
presence of hyper-segmented neutrophils. Lupus screens, copper
levels, zinc levels, faecal elastase and coeliac screens were all ei-
ther negative or normal. An MRI of the spine showed signal in the
upper thoracic region which was compatible with B12 deficiency.
A repeat upper endoscopy with multiple biopsies did not reveal
any sign of atrophic gastritis or coeliac disease. The patient was
reviewed by a dietian who confirmed that the gastrojejunostomy
tube was a recognized cause of B12 deficiency. The patient was
started on an injection of hydroxycobalamin. The registrar called
for an interdisciplinary round with all physicians involved in the
patient’s care, to further discuss the patient’s future management.
Advice from a movement disorder specialist was sought to dis-
cuss options for devices to assist medication delivery. The patient
was tried on a continuous apomorphine infusion and carbidopa/
levodopa intestinal gel via a percutaneous gastrostomy tube. The
last option was deep brain stimulation which usually works well
for tremor dominant Parkinsonism and is a good way to reduce
the need for medications. The patient and family decided to con-
tinue on the continuous apomorphine infusion and indefinite B12
injections.
3. Acute Presentations of Parkinsonism
Most complications are either associated with the progress of Par-
kinson’s disease or side-effects of the medication. Many of these
complications can be dealt with in an outpatient clinic, but it is not
uncommon for a patient with Parkinsonism to present to the ED
for urgent management and inpatient admission. Dyskinesia is a
very common complication which occurs at peak dose of medi-
cation, or during a prolonged “off” [1] or delayed “on” periods. It
is often managed in the outpatient setting. Patients may also ex-
perience symptoms such as visual hallucinations and rarely audi-
tory hallucinations, paranoid delusions, weight loss, agitation and
a hyperactive delirium. An inpatient admission and assessment is
very important to consider reduction of medications such as anti-
cholinergics, mono-amine oxidase inhibitors, dopamine agonists,
COMT inhibitors, levodopa, and all other dopaminergic, opioid
and tricyclic antidepressants. Atypical antipsychotics such as que-
tiapine or clozapine should be introduced in conjunction with a
psychiatrist and a movement disorder specialist [2-4]. Typical an-
tipsychotics may precipitate neuroleptic malignant syndrome. A
cholinesterase inhibitor may reduce visual hallucinations and psy-
chosis [5] impulse control problems, and dopamine dysregulation
syndrome. Urgent involvement of a movement disorder specialist
to reduce dopamine agonists, device-assisted medications such as
continuous apomorphine infusions, levodopa–carbidopa intestinal
gel or deep brain stimulation of the subthalamic nucleus may be
of benefit [6].
http://acmcasereports.com 3
Volume 8 Issue 9 -2022 Case Report
4. Dysphagia Causing Severe Malnutrition and Aspira-
tion Pneumonia
An inpatient admission for video fluoroscopy and involvement of
an allied health specialist such as a speech therapist to discuss de-
vice-assisted therapy may be required to assess dysphagia. Intesti-
nal pseudo-obstruction and paralytic ileus, may be considered after
excluding organic obstructions. Prokinetic medications may be an
alternative treatment. Dopamine inhibitors should be avoided.
5. Syncope Due to Orthostatic Hypotension
Patient admissions are mandatory to review medications and with-
hold any medications which may cause orthostatic hypotension,
such as dopamine agonists, monoamine oxidase inhibitors and any
antihypertensive medication. Fludrocortisone or midodrine may
also be considered to raise the blood pressure [7].
6. Parkinsonism-Hyperpyrexia Syndrome
Akinesis and fever may occur due to medication non-compliance.
Complications may include acute renal failure, aspiration pneumo-
nia and venous thromboembolism. Management involves dopami-
nergic drug administration, treating symptoms, and preventing
complications of disease [8]. The patient should be managed in the
ICU with continuous monitoring. Multidisciplinary care should
be provided. Refractory cases may require oral sodium dantrolene
and bromocriptine, intravenous amantadine, and in refractory cas-
es, pulsed methyl-prednisolone [8].
7. Serotonin Syndrome
Patients with Serotonin Syndrome usually present with severe
akathisia, myoclonus, mydriasis, diarrhoea, fever, confusion
and hypertonia. It usually occurs following administration of a
MAO-inhibitor, tricyclic antidepressant or morphine. Hyper-se-
rotonin syndrome is due to stimulation of postsynaptic serotonin.
Patients should receive medical care in the ICU [9].
8. Falls
Falls are a serious complication of medications, reduced mobility,
orthostatic hypotension, impaired postural reflexes and increased
‘off’ periods due to progression of disease [10], such as rigidity
and gait ‘freezing’. Patients may develop serious fractures. Falls
are a common cause for admission to a residential home as patients
often need 24-hour care following falls [11].
9. REM Sleep Disorder
Rapid eye movement sleep disorder is characterised by patients
vigorously acting out dreams. This may result in harm to their part-
ner. A small dose of clonazepam may be useful for this.
10. Conclusion
Parkinsonism is a movement disorder disease where patients are
cared for by a multidisciplinary team. Although most decisions are
made in outpatient clinics, patients commonly present acutely to
ED due to falls, serious fractures, medication complications, and
disease progression. Despite medications, patients may lose their
independence and require ACAT assessment or assessment for res-
idential care [12].
References
1. Calabresi P, Di Filippo M, Ghiglieri V, Tambasco N, Picconi BJTLN.
Levodopa-induced dyskinesias in patients with Parkinson’s disease:
filling the bench-to-bedside gap. 2010; 9(11): 1106-17.
2. Goldman JG, Holden SJCtoin. Treatment of psychosis and dementia
in Parkinson’s disease. 2014; 16(3): 281.
3. Olanow CW, Stocchi F, Lang A. Parkinson’s disease: non-motor and
non-dopaminergic features: John Wiley & Sons. 2011.
4. Friedman JHJP, disorders r. Parkinson’s disease psychosis 2010: a
review article. 2010; 16(9): 553-60.
5. Goldman JG, Vaughan CL, Goetz CGJEoop. An update expert opin-
ion on management and research strategies in Parkinson’s disease
psychosis. 2011; 12(13): 2009-24.
6. Williams DR, Evans AH, Fung VS. Practical approaches to com-
mencing device‐assisted therapies for Parkinson disease in Austra-
lia. 2017; 47(10): 1107-13.
7. Sánchez-Ferro Á, Benito-León J, Gómez-Esteban JCJFin. The man-
agement of orthostatic hypotension in Parkinson’s disease. 2013; 4:
64.
8. Newman EJ, Grosset DG, Kennedy PGE. The Parkinsonism-Hyper-
pyrexia Syndrome. Neurocritical Care 2009; 10(1): 136-40.
9. R Suratos CT, Del Rosario MM, G Jamora RDJNDM. Serotonin
syndrome in a Parkinson disease patient after intake of an etha-
nol-containing homeopathic medication. 2020; 10(4): 219-22.
10. Zhang L-L, Canning SD, Wang X-PJCn. Freezing of gait in Parkin-
sonism and its potential drug treatment. 2016; 14(4): 302.
11. Worthington JM, Ney J. The end of life with PD can be well-lived:
The neurologist’s role. AAN Enterprises. 2015.
12. Safarpour D, Thibault DP, DeSanto CL. Nursing home and end-of-
life care in Parkinson disease. 2015; 85(5): 413-9.

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Emergencies In Parkinsonism

  • 1. Annals of Clinical and Medical Case Reports Case Report ISSN: 2639-8109 Volume 8 Emergencies in Parkinsonism Adel Ekladious1* and Ramana Waran2 1 Faculty of Health and Medical Sciences, University of Western Australia, 35 Stirling Hwy, Crawley, WA, Australia, South East Region- al Hospital, 4 Virginia Drive, Bega, NSW, Australia 2 University of Wollongong (UOW), School of Medicine, NSW, Australia, Cass Byres ( Medical student) UOW , school of medicine , NSW, Australia * Corresponding author: Adel Ekladious, Faculty of Health and Medical Sciences, University of Western Australia, 35 Stirling Hwy, Crawley, WA, Australia, South East Regional Hospital, 4 Virginia Drive, Bega, NSW, Australia, E-mail: ekladiou@gmail.com Received: 29 Jan 2022 Accepted: 07 Feb 2022 Published: 14 Feb 2022 J Short Name: ACMCR Copyright: ©2022 Adel Ekladious. This is an open access article dis- tributed under the terms of the Creative Commons Attribu- tion License, which permits unrestricted use, distribution, and build upon your work non-commercially. Citation: Adel Ekladious, Emergencies in Parkinsonism. Ann Clin Med Case Rep. 2022; V8(9): 1-3 1. Abstract Patients with Parkinsonism may present acutely to the ED with serious and even life-threatening conditions. Although falls are a common presentation in advanced Parkinsonism, early presen- tations with falls should alert the clinician that the patient might have a Parkinson syndrome other than Parkinson’s disease itself, including autonomic neuropathy causing orthostatic hypotension. Patients may present with neuroleptic malignant syndrome, acute psychosis, marked hypokinesis, freezing gait, aspiration pneumo- nia, dysphagia, serotonin syndrome, dopamine dysregulation syn- drome and intestinal pseudo-obstruction.An inpatient admission is necessary for investigation and observation of these patients. We present a case of a patient who presented with an uncommon side effect of a common medication used for Parkinsonism. 2. Case Report A 60-year-old man presented with weakness leading a fall and subsequent fracture of his left arm. His medical history was signif- icant for Parkinsonism, diagnosed at the age of 50. He was being followed-up regularly by a movement disorder specialist every three months. His medications included levodopa/carbidopa 750 mg daily, rotigotine dermal patch 6 mg daily and amantadine 300 mg daily for one year. He started to develop motor fluctuations of delayed ‘on’ and unpredictable ‘off’ periods and painful dyskine- sia. The patient’s partner reveled to his specialist that he had also started to develop non-motor symptoms of a Rapid Eye Movement disorder, where the patient started to enact his dreams by punching his partner. Clonazepam did not improve his symptoms, but mela- tonin did to moderate effect. The patient started to experience gait freezing and dyskinesia, so rotigontine was ceased and levodopa/ carbidopa was increased to one gram daily. A MAO inhibitor and COMT inhibitor were added with no improvement. 18 months ago, he was started on intermittent apomorphine SC by his specialist with significant symptomatic improvement. He was subsequent- ly started on a continuous infusion of apomorphine 4mg/hour 6 months later. His sleep improved significantly. When he presented to the ED, examination by an Advanced Trainee revealed that the ‘pull-test’ was positive and the patient looked jaundiced and pale. The remainder of the examination, including the chest, abdomen, lymph nodes, muscles and joints, were unremarkable. There was no postural hypotension, no tremor, and no rigidity. The patient had a chest X-ray and an ECG which showed no abnormal findings apart from fracture in the left clavicle. An orthopedic Registrar reviewed the patient and advised for symptomatic management of Parkinsonism. A movement specialist nurse advised for the patient to continue on the same medications. In the ED, the Haemoglo- bin was 7 grams/DI, Haematocrit 19, MCV 95, Platelets 190, AST 30, total bilirubin 4, and unconjugated bilirubin 3. The patient was given 3 units of packed red cells. Gastroenterology booked the pa- tient for an upper and lower endoscopy the following day, which did not show any signs of bleeding. On Day 3 the Senior Registrar received a call from haematology. They informed the treating team that the patient had a high LDH, low haptoglobin and spherocy- tosis on the blood film. Serum electrophoresis did not show clon- ality. Serum B12, folate and copper were normal. Methylmalonic acid, homocysteine, zinc levels, immunoglobulin, immunopheno- typing, the kappa/lambda ratio, flow cytometry, serum nitric oxide, and G6PD levels were also normal. Haemoglobin electrophoresis http://acmcasereports.com 1
  • 2. http://acmcasereports.com 2 Volume 8 Issue 9 -2022 Case Report showed normal HbA2 and no evidence of thalassemia or sickle cell anemias. An immune screen, including ANA, ENA, Coombs’ test, Anti-Scl-70, Anti-RPN, rheumatoid factor, complement, an- ti-CCP, and an anti-synthetase screen were all either negative or normal. A CT head, neck, chest, abdomen, pelvis, and ultrasound of the testes were also all normal. The patient was reassured and sent home with plans for a follow-up with his specialist and the orthopaedic team as an outpatient. The patient’s specialist advised for the patient to continue on his medication for Parkinson’s as it appeared to be working well to control his symptoms. Two weeks later, the patient presented to the ED after having another fall. The cause of the fall was unclear. His Haemoglobin had dropped to 5 grams/DI, and the patient had an elevated AST, LDH and uncon- jugated bilirubin. The haematology registrar was called to look at the peripheral blood film, and he confirmed that the patient had a hemolytic anemia. In consultation with his consultant, the regis- trar advised to send the patient to the haematology department for consideration of a bone marrow biopsy. The patient’s movement disorder specialist advised for him to continue taking the same medication. The patient was reviewed by cardiology who advised that the patient should continue on telemetry and should arrange for a transthoracic echocardiogram. Four units of packed red cells were infused. The patient later had a bone marrow biopsy which showed normal erythropoiesis. An echocardiogram was performed which showed normal muscles and valves, and there was normal cardiac systolic and diastolic function. The patient was eventual- ly seen by the consultant hematologist who examined the patient and his blood film diagnosed them with drug-associated bite cell hemolytic anemias. His medication was reviewed by the pharma- cist and immunologist, who agreed that the patient had a hemolyt- ic anemia due to apomorphine. The apomorphine was ceased in consultation with his specialist. The patient was seen by his neu- rologist and specialist nurse. In consultation with the patient, it was decided that the patient was to receive levodopa/carbi-dopa intestinal infusion gel. The patient had a percutaneous endoscopic gastrostomy into the jejunum with 2 grams of levodopa and 500 mg carbidopa. Patient complications such as dislodgement of the jejunal tube, catheter migration, bezoar formation, intestinal ob- struction, abdominal pain, flatulence and constipation were all ex- plained to the patient. The patient was discharged home with plans for outpatient reha- bilitation and follow-up with a specialist Parkinsonism nurse. 10 months later, the patient attended the ED because he could not feel his legs and had had a fall. The patient was admitted to an acute assessment unit. They were seen by neurology, who performed an EMG and diagnosed the patient to have a peripheral sensory neu- ropathy. His blood tests confirmed the patient had a haemolytic anaemia, however there was no clear cause to explain the haemolysis. The patient was transfused with 3 units of packed RBC. His serum B12 was 12 (300-600), folate was within normal limits and homocys- teine and MMA were elevated. A bone marrow biopsy confirmed presence of hyper-segmented neutrophils. Lupus screens, copper levels, zinc levels, faecal elastase and coeliac screens were all ei- ther negative or normal. An MRI of the spine showed signal in the upper thoracic region which was compatible with B12 deficiency. A repeat upper endoscopy with multiple biopsies did not reveal any sign of atrophic gastritis or coeliac disease. The patient was reviewed by a dietian who confirmed that the gastrojejunostomy tube was a recognized cause of B12 deficiency. The patient was started on an injection of hydroxycobalamin. The registrar called for an interdisciplinary round with all physicians involved in the patient’s care, to further discuss the patient’s future management. Advice from a movement disorder specialist was sought to dis- cuss options for devices to assist medication delivery. The patient was tried on a continuous apomorphine infusion and carbidopa/ levodopa intestinal gel via a percutaneous gastrostomy tube. The last option was deep brain stimulation which usually works well for tremor dominant Parkinsonism and is a good way to reduce the need for medications. The patient and family decided to con- tinue on the continuous apomorphine infusion and indefinite B12 injections. 3. Acute Presentations of Parkinsonism Most complications are either associated with the progress of Par- kinson’s disease or side-effects of the medication. Many of these complications can be dealt with in an outpatient clinic, but it is not uncommon for a patient with Parkinsonism to present to the ED for urgent management and inpatient admission. Dyskinesia is a very common complication which occurs at peak dose of medi- cation, or during a prolonged “off” [1] or delayed “on” periods. It is often managed in the outpatient setting. Patients may also ex- perience symptoms such as visual hallucinations and rarely audi- tory hallucinations, paranoid delusions, weight loss, agitation and a hyperactive delirium. An inpatient admission and assessment is very important to consider reduction of medications such as anti- cholinergics, mono-amine oxidase inhibitors, dopamine agonists, COMT inhibitors, levodopa, and all other dopaminergic, opioid and tricyclic antidepressants. Atypical antipsychotics such as que- tiapine or clozapine should be introduced in conjunction with a psychiatrist and a movement disorder specialist [2-4]. Typical an- tipsychotics may precipitate neuroleptic malignant syndrome. A cholinesterase inhibitor may reduce visual hallucinations and psy- chosis [5] impulse control problems, and dopamine dysregulation syndrome. Urgent involvement of a movement disorder specialist to reduce dopamine agonists, device-assisted medications such as continuous apomorphine infusions, levodopa–carbidopa intestinal gel or deep brain stimulation of the subthalamic nucleus may be of benefit [6].
  • 3. http://acmcasereports.com 3 Volume 8 Issue 9 -2022 Case Report 4. Dysphagia Causing Severe Malnutrition and Aspira- tion Pneumonia An inpatient admission for video fluoroscopy and involvement of an allied health specialist such as a speech therapist to discuss de- vice-assisted therapy may be required to assess dysphagia. Intesti- nal pseudo-obstruction and paralytic ileus, may be considered after excluding organic obstructions. Prokinetic medications may be an alternative treatment. Dopamine inhibitors should be avoided. 5. Syncope Due to Orthostatic Hypotension Patient admissions are mandatory to review medications and with- hold any medications which may cause orthostatic hypotension, such as dopamine agonists, monoamine oxidase inhibitors and any antihypertensive medication. Fludrocortisone or midodrine may also be considered to raise the blood pressure [7]. 6. Parkinsonism-Hyperpyrexia Syndrome Akinesis and fever may occur due to medication non-compliance. Complications may include acute renal failure, aspiration pneumo- nia and venous thromboembolism. Management involves dopami- nergic drug administration, treating symptoms, and preventing complications of disease [8]. The patient should be managed in the ICU with continuous monitoring. Multidisciplinary care should be provided. Refractory cases may require oral sodium dantrolene and bromocriptine, intravenous amantadine, and in refractory cas- es, pulsed methyl-prednisolone [8]. 7. Serotonin Syndrome Patients with Serotonin Syndrome usually present with severe akathisia, myoclonus, mydriasis, diarrhoea, fever, confusion and hypertonia. It usually occurs following administration of a MAO-inhibitor, tricyclic antidepressant or morphine. Hyper-se- rotonin syndrome is due to stimulation of postsynaptic serotonin. Patients should receive medical care in the ICU [9]. 8. Falls Falls are a serious complication of medications, reduced mobility, orthostatic hypotension, impaired postural reflexes and increased ‘off’ periods due to progression of disease [10], such as rigidity and gait ‘freezing’. Patients may develop serious fractures. Falls are a common cause for admission to a residential home as patients often need 24-hour care following falls [11]. 9. REM Sleep Disorder Rapid eye movement sleep disorder is characterised by patients vigorously acting out dreams. This may result in harm to their part- ner. A small dose of clonazepam may be useful for this. 10. Conclusion Parkinsonism is a movement disorder disease where patients are cared for by a multidisciplinary team. Although most decisions are made in outpatient clinics, patients commonly present acutely to ED due to falls, serious fractures, medication complications, and disease progression. Despite medications, patients may lose their independence and require ACAT assessment or assessment for res- idential care [12]. References 1. Calabresi P, Di Filippo M, Ghiglieri V, Tambasco N, Picconi BJTLN. Levodopa-induced dyskinesias in patients with Parkinson’s disease: filling the bench-to-bedside gap. 2010; 9(11): 1106-17. 2. Goldman JG, Holden SJCtoin. Treatment of psychosis and dementia in Parkinson’s disease. 2014; 16(3): 281. 3. Olanow CW, Stocchi F, Lang A. Parkinson’s disease: non-motor and non-dopaminergic features: John Wiley & Sons. 2011. 4. Friedman JHJP, disorders r. Parkinson’s disease psychosis 2010: a review article. 2010; 16(9): 553-60. 5. Goldman JG, Vaughan CL, Goetz CGJEoop. An update expert opin- ion on management and research strategies in Parkinson’s disease psychosis. 2011; 12(13): 2009-24. 6. Williams DR, Evans AH, Fung VS. Practical approaches to com- mencing device‐assisted therapies for Parkinson disease in Austra- lia. 2017; 47(10): 1107-13. 7. Sánchez-Ferro Á, Benito-León J, Gómez-Esteban JCJFin. The man- agement of orthostatic hypotension in Parkinson’s disease. 2013; 4: 64. 8. Newman EJ, Grosset DG, Kennedy PGE. The Parkinsonism-Hyper- pyrexia Syndrome. Neurocritical Care 2009; 10(1): 136-40. 9. R Suratos CT, Del Rosario MM, G Jamora RDJNDM. Serotonin syndrome in a Parkinson disease patient after intake of an etha- nol-containing homeopathic medication. 2020; 10(4): 219-22. 10. Zhang L-L, Canning SD, Wang X-PJCn. Freezing of gait in Parkin- sonism and its potential drug treatment. 2016; 14(4): 302. 11. Worthington JM, Ney J. The end of life with PD can be well-lived: The neurologist’s role. AAN Enterprises. 2015. 12. Safarpour D, Thibault DP, DeSanto CL. Nursing home and end-of- life care in Parkinson disease. 2015; 85(5): 413-9.