HISTORY COLLECTION

IDENTIFICATION DATA

Name of the patient: - Mrs. Shanta Ninjoor.

Age: - 78 years/ Female
Ip No./MRD No.: -1429024/398796
Name of the Ward: - Intensive Care Unit.
Doctor’s Unit: -Dr. Nikhil Shah.
Educational Status: - Studied till 10th Standard+.
Occupation: - Unemployed.
Marital Status: - Widow.
Address: - Sundarvan Society, Silvassa.
Date of admission: - 16/06/2021.
Diagnosis: - Iron Deficiency Anemia with K/C/O Parkinson’s disease.
Date of Surgery: - Not performed.
Name of Surgery: - Not applicable.
Post-Operative Day: - Not applicable.

Chief Complaints:
 Patient was having generalized weakness
 Loss of appetite
 Tremors in hands and legs
 Difficulty in swallowing
 Unable to speak properly due to slurring of speech
 Unable to walk and stand without support
 Constipation for 2 days
History of complaints during the time of admission: -
Sr. Major Complaints Duration Treatment Provided

1. Giddiness Since Inj. Augmentin 1.2 gm IV TDS

2. Weakness one week Inj. Levofloxacin 200 mg IV OD
Inj. Pantoprazole 40 mg IV OD
Inj. Emset 4 mg IV TDS
Inj. Mucinac 600 mg SOS
Tab. Lasilactone 20/50 mg BD
Tab. Telma 20 mg OD
Tab. Alprax 0.25 mg HS
Tab. Calaptin SR OD
Tab. Syndopa Plus QID
Tab. Pramipexole 0.5mg TDS

Past Medical history: -

K/H/O Parkinsonism for 10 years
K/H/O Hypertension for 20 years
H/O Repeated blood transfusion every 2-3 months

Past Surgical history: -

Patient did not underwent any surgical procedure in past.

Present Medical History: -

Patient is having Iron Deficiency Anemia

Present Surgical History :-

No any surgery performed.
 Family Pedigree :-

FATHER
MOTHER

CLIENT
HUSBAND

SON SON

KEYWORDS

-MALE

-FEMALE

-CLIENT

-DEATH
 Family Information: -
Relatio
Name of nship
Marital Health
Sr. Family with Age Education Occupation
Status Status
members the
client
Lt. Mr.
Ambare He was
1. Father ----- ------------- --------- Died
sh Illiterate
Ninjoor
Lt. Mrs.
She was
2. Janki Mother ---- ----------- ---------- Died
illiterate
Ninjoor
Lt. Mr.
Husban He was a
3. Basavaraja ----- ------- ------- Died
d clerk
Ninjoor
Mrs.
78 Unhealt
4. Shanta Client Graduate Home maker Widow
years hy
Ninjoor
Mr.
Husban 50
5. Madhava Graduate Worker Married Healthy
d years
Ninjoor
Mr.
Husban 48
6. Ghatam Graduate Worker Married Healthy
d years
Ninjoor

Family Health History: - No other members have health problems except

client

Personal History: -
Habits: - No any bad habits of drinking alcohol, smoking or chewing tobacco.
Allergy: - No any specific allergy to drug, pollen or insects.
Lifestyle/High risk behavior: - Sedantary lifestyle
Sleeping pattern: - Sleeps 6-8 hours at night.
Dietary pattern: - Eats three times meal a day but in less quantity, and follows
a non-vegetarian diet.
Bowel & bladder pattern: - Passes stool one time and urine 4-5 times a day.
Food hygienic practices: - Washes fruits and vegetables before cooking.
Skin Conditions
 Color: Pale
 Moisture: Skin is moist
 Temperature: Afebrile
 Turgor: Present
 Edema: Bilateral pedal edema present (Non-pitting)
 Lesions: Not present

Vital Signs: -
Temperature 97.4o F
Pulse 82 beats/minute
Respiration 18 breath/minute
Blood Pressure 130/80 mmHg
Pain 4/10
SpO2 96% with 4 liters O2
Level of Consciousness Fully Conscious
Urine Output 1200 ml/day

HEAD TO TOE ASSESSMENT

Head
Scalp
Inspection
 Shape of the skull: Normal in shape
 Scalp: Clear, no any dandruff present
 Hair: Black in color
Palpation
No any tenderness present on palpating head.

Face
Inspection: - Patient looks anxious and worried.
Palpation: - No any tenderness present on palpating face.

Eyes: -
Inspection
Any disease: - No any disease present like stye, conjunctivitis, etc.
Conjunctiva: - Pale in color
Sclera: White in color
Pupils: Pupils equally round and reacting to light and accommodation.
Visual Acuity: Normal
Visual fields: All visual fields are normal
Ocular movements: Normal
Lacrymal glands: Normal
Cornea: Transparent
Vision: Presbyopia present

Ears
External ear: - Normal in shape
Tympanic membrane: Earwax present
Hearing tests:
Weber’s test: Not able to hear in both ears
Rinnie’s test: Not able to hear in both ears

Nose
External Nares: Normal in shape, no any nasal deviation present.
Nostrils: Normal
Patency: Patent airway no any occlusion present
Olfactory sense: Smell sensation is present

Mouth and pharynx

Lips: Pink in color
Buccal Mucosa: No any stomatitis present
Gums: No any gingivitis present
Teeth: Dental caries present (1 tooth in left side)
Palates and uvula: Normal
Tonsil areas: Normal, no tonsillitis present
Tongue: Pale
Voice: No any hoarseness present
Taste: Taste sensation present
Trachea: Trachea is in midline
Thyroid: No any inflammation present
Muscles: No any inflammation present
Carotid arteries: Bilaterally equally palpable
Jugular venous distension: Jugular distension not present

Chest and Respiratory System

Inspection
Chest shape: Normal size and shape
Type of Respiration: Dyspnea without O2 support
Chest expansion: Bilaterally equal

Palpation
Fremitus: Present
General Palpation: No any tenderness present
Breast: Flat
Lymph Node: No any lymph node enlargement

Percussion
Resonance present

Auscultation
Normal Breath sounds: Not heard
Adventitious sounds: wheezing heard
Heart sounds: Present
S1: Heard
S2: Heard

Abdomen:
Inspection: Normal in shape
Auscultation: Bowel sound present
Palpation: No any tenderness present
Percussion: Tympany present

Back :
Spina Bifida: Not present
Curves: Normal

GENITOURINARY SYSTEM
Kidney: Not palpable
Bladder: Not palpable
Hernias: Not present
Masses: Absent
Genitalia and area nodes : Not present

Rectal examination :
No any fissure or hemorrhoids present

Extremities :
Movement of joints: Painful on doing range of motion exercises.
Tremors: Present
Clubbing of fingers: Not present
Ankle edema: Not present
Varicose Veins: Not present

Neurological tests:
Motor Coordination: Not present, unable to stand still to walk
Equilibrium tests: Not present

Reflexes
Biceps:
Triceps:
Patellar: Not performed
Achilles:
Plantar:
Tests for sensation: Hot and cold sensation present
 LABORATORY INVESTIGATIONS

Date/Time Name of the Patient’s Normal Inference

Investigations Value Values
16/06/2021 Blood Group O positive ---- ----
16/06/2021 Hemogram CBC
Hb 5.1gms% 12-17.5 Low
TLC 4.5/cumm 4.0-10.0 Normal
RBC 1.32 mill/cum 3.6-5.6 Normal
PCV 14.2% 42-52 Low
MCV 108 fl 82-98 Low
MCH 38.6 pg/ml 23-34 Low
MCHC 35.9 gm/dl 32-37 Low
PLT 3.1lac/cumm 1.5-4.5 Low
POLYS 68% 50-60 High
LYMPHO 28% 20-40 Normal
EOSINO 02% 1-8 Normal
MONO 02% 2-6 Normal
BASO 00% 0-1 Normal
Blood Urea Nitrogen 17 mg/dl
SERUM BILIRUBIN
S. bilirubin total 0.5 mg/dl 0.2-1 Normal
S. bilirubin direct 0.2 mg/dl 0-0.2 Normal
S. bilirubin indirect 0.3 mg/dl 0-0.8 Normal
S.G.P.T 15 0-42 Normal
S.G.O.T 26 0-42 Normal
S. Alkaline Phosphatase 163 IU/L 25-150 Normal
PT/INR
TEST 12.1 sec 10.5-14.5 Normal
CONTROL 11.8 sec 0-12.5 Normal
INR 0.9 0.8-1.2 Normal
22/06/2021 SERUM
ELECTROLYTES
Serum Sodium 130mEq/L 135-150 Normal
Serum Potassium 4.5mEq/L 3.5-5.5 Normal
Serum Chloride 86mEq/L 94-110 Normal

ESR 52mm/1hr 1-7 High

SERUM PROTEINS
Albumin 3.2gm/dl 3.5-5 Low
A/G Ratio 0.7

Serum Creatinine 0.9 mg/dl 0.7 to 1.3 Normal

ABG ANALYSIS
Blood Gas Values
pH 7.224
pCO2 49.5
pO2 29.8
Oximetry Values
ctHb 12.0g/dl
sO2 31.0%
FO2Hb 30.6%
FMetHb 0.9%
FCOHb 0.3%
FHHb 68.2%
Electrolyte Values
cK+ 4.0mmol/L
cNa+ 145mmol/L
cCa2+ 0.78mmol/L
cCl- 116mmol/L
Temperature Corrected
Values
pH(T) 7.224
pCO2(T) 49.5mmHg
pO2(T) 29.8mmHg
Acid base Status
CtO2 2.3mmol/L
 cBase(Ecf)c -6.7mmol/L
AnionGap, K+c 13.4mmol/L
cHCO3-(P)C 19.7mmol/L
cCa2+(7.4)c 0.71mmol/L
Hctc 37.0%

17/06/2021 Serum Iron 200.38 mg/dl 37-45 High

TIBC 202.48 mg/dl 250-450 Low
Transferrin Saturation 98.96 % 20-60 High

16/06/2021 HRCT THORAX

Few atelactic bands in basal segments of right lower lobe
Mild calcification of aortic valve, aorta and coronary vessels

MEDICATIONS: -

a) Inj. Augmentin 1.2 gm IV TDS

b) Inj. Levofloxacin 200 mg IV OD
c) Inj. Pantop 40 mg IV OD
d) Inj. Emset 4 mg IV TDS
e) Inj. Mucinac 600 mg SOS
f) Tab. Lasilactone 20/50 mg BD
g) Tab. Telma 20 mg OD
h) Tab. Alprax 0.25 mg HS
i) Tab. Calaptin SR OD
j) Tab. Syndopa Plus QID
k) Tab. Pramipexole 0.5mg TDS
 ANATOMY AND PHYSIOLOGY OF BASAL
GANGLIA
Parkinson’s Disease is considered predominantly a disorder of the basal
ganglia.

The basal ganglia are a group of nuclei situated deep and centrally at the
base of the forebrain. They have robust connections with the cerebral
cortex and thalamus in addition to other areas of the brain. Their vast
system of communication allows them involvement with a variety of
functions, including automatic and voluntary motor control, procedural
learning relating to routine behaviours and emotional functions. The
association with other cortical areas ensures smoothly orchestrated
movement control and motor behaviour.

The striatum, composed of the caudate and putamen, is the largest nuclear
complex of the basal ganglia. The striatum receives excitatory input from
several areas of the cerebral cortex, as well as inhibitory and excitatory
input from the dopaminergic cells of the substantia nigra pars compacta
(SNc). These cortical and nigral inputs are received by the spiny projection
neurons, which are of 2 types:
 1. Those that project directly to the internal segment of the
globus pallidus (GPi), the major output site of the basal
ganglia. The consequence of this pathway is to increase the
excitatory drive from thalamus to cortex i.e. as the motor
cortex increases firing rates, this results in increased activity in
the corticospinal tract and eventually the muscles, so ‘turns up’
the action of the motor system.
2. Those that project to the external segment of the globus
pallidus (GPe), establishing an indirect pathway to the GPi via
the subthalamic nucleus (STN). The consequence of the
indirect pathway is to decrease the excitatory drive from
thalamus to cortex. The increase in inhibition of the thalamic
neurons in effect ‘turns down’ motor activity from the cortex
The actions of both pathways regulate the neuronal output from the GPi,
thus providing tonic inhibitory input to the thalamic nuclei that project to
the primary and supplementary motor areas.

DIVISIONS OF THE BASAL GANGLIA

1. Corpus Striatum- (The largest subcortical brain structure of

the basal ganglia is the striatum with a volume of
approximately 10 cm). It is a heterogeneous structure that
receives afferents from several cortical and subcortical
structures and projects to various basal ganglia nuclei. [1] Within
the striatum, there are two main divisions
 Dorsal striatum (DS) see image, shown in red.
Primarily involved in control over conscious motor
movements and executive functions.
The dorsal striatum consists of the caudate
nucleus and the putamen. A white matter, nerve
tract (the internal capsule) in the dorsal striatum
separates the caudate nucleus and the putamen.
  Ventral striatum, responsible for limbic functions of
reward and aversion. Consists of nucleus accumbens
and the olfactory tubercle. [2]

2. Internal and External segments of Globus Pallidus

(NB until the first half of the 19th century the globus pallidus
and putamen were considered one structure, collectively
referred to as the lentiform or lenticular nucleus[3])
3. Subthalamic Nucleus (STN) - a lens-shaped cell group that
makes up the largest part of the subthalamus
4. Substantia Nigra (SN) - (“black substance” in Latin) is a
long nucleus located in the midbrain but considered
functionally a part of the basal ganglia because of its reciprocal
connections with other brainstem nuclei. It consists of two
components, the pars compacta and the pars reticulata, which
have different connections and use
different neurotransmitters. [4] The 2 minute video below
outlines BG concepts

PHYSIOLOGY OF DOPAMINE
Dopamine controls various physiological functions in the brain and
periphery by acting on its receptors D1, D2, D3, D4, and D5. Dopamine
receptors are G protein–coupled receptors involved in the regulation of motor
activity and several neurological disorders such as schizophrenia, bipolar
disorder, Parkinson’s disease (PD), Alzheimer’s disease, and
attention-deficit/hyperactivity disorder. Reduction in dopamine content in the
nigrostriatal pathway is associated with the development of PD, along with the
degeneration of dopaminergic neurons in the substantia nigra region. Dopamine
receptors directly regulate neurotransmission of other neurotransmitters, release
of cyclic adenosine

Receptor D1 D5 D2 D3 D4
s

Location Striatum, Cortex, Striatum, Striatum, Frontal

nucleus substantia VTA islands of cortex,
accumbens. nigra, Olfactory Calleja, amygdala,
Olfactory hypothala bulb, cortex hypothalam
bulb, cerebral us, nucleus
 amygdala mus cortex accumbens
hippocampu
s, substantia
nigra
Hypothalam
us, frontal
cortex

Type Gs-coupled Gs-coupled Gi-coupled Gi- Gi-coupled

coupled

Mechani Increased Adenylate Increased Adenylate Adenylate

sm intracellular cyclase↑ intracellula cyclase↓ cyclase↓
level of r level of
cAMP by cAMP by
activated activate
adenylate adenylate
cyclase cyclase

Function Locomotion Cognition, Locomotio Locomoti Cognition,

, learning attention, n, learning on, impulse
and decision and cognition, control,
memory, making, memory, attention, attention,
attention, motor attention, impulse sleep,
impulse learning, sleep, control, reproductiv
control, renin reproductiv sleep, e behavior
sleep, secretion e behaviour regulation
regulation of food
of renal intake
function
 Selective SKF-38393 — Bromocript 7-OH- A-412997
agonist SKF-81297 ine DPAT ABT-670
Fenoldopam Pergolide Pramipex PD-168077
(SKF- Cabergolin ole
82526) e Rotigotine
Ropinirole PD-
128907

Selective SCH-23390 — Haloperidol Nafadotri A-381393

antagoni SCH-39166 Raclopride de GR- FAUC213
st SKF-83566 Sulpiride 103691 L-745870
Spiperone GR- L-750667
Risperidon 218231
e SB-
277011A
NGB-
2904 PG-
01037
ABT-127

monophosphate, cell proliferation, and differentiation. Here, we provide an

update on recent knowledge about the signalling mechanism, mode of action,
and the evidence for the physiological and functional basis of dopamine
receptors. We also highlight the pivotal role of these receptors in the modulation
of neurogenesis, a possible therapeutic target that might help to slow down the
process of neurodegeneration.
 DISEASE CONDITION

PARKINSON’S DISEASE

INTRODUCTION

Parkinson’s disease is a slowly progressing neurologic

movement disorder that eventually leads to disability. It is the fourth
most common neurodegenerative disease, and 50,000 new cases are
reported each year in the United States (Chen & Fernandez, 2007;
Thomure, 2006). The disease affects men more often than women.
Symptoms usually first appear in the fifth decade of life; however,
cases have been diagnosed as early as 30 years of age. The
degenerative or idiopathic form of Parkinson’s disease is the most
common; there is also a secondary form with a known or suspected
cause.
Although the cause of most cases is unknown, research suggests
several causative factors, including genetics, atherosclerosis,
excessive accumulation of oxygen free radicals, viral infections, head
trauma, chronic use of antipsychotic medications, and some
environmental exposures.

DEFINITION: -

EPIDEMIOLOGY: -
Parkinson's disease (PD) affects 1-2 per 1000 of the population at any
time. PD prevalence is increasing with age and PD affects 1% of the
population above 60 years. The main neuropathological finding is α-
synuclein-containing Lewy bodies and loss of dopaminergic neurons
in the substantia nigra, manifesting as reduced facilitation of
voluntary movements. With progression of PD, Lewy body pathology
spreads to neocortical and cortical regions.

ETIOLOGY/RISK FACTORS: -

BOOK PICTURE PATIENT PICTURE

PD is a multifactorial disease, with Patient was having Parkinson due to

both genetic and environmental unknown etiology
factors playing a role. Age is the
biggest risk factor for PD, with the
median age of onset being 60 years of
age

Cigarette smoking
Cigarette smoking has been
extensively studied with respect to
PD, with mostly consistent results.
Most of the epidemiological reports
are case-control studies showing a
reduced risk of developing PD, with
larger cohort studies also in
agreement

Caffeine
Several studies have investigated the
effect of caffeine on the development
of PD and reported a reduced risk of
developing PD among coffee
drinkers.

Pesticides, herbicides, and heavy

metals
In 1983, 1-methyl-4-phenyl-1,2,3,6-
tetrahydropyridine (MPTP) was first
discovered to be associated with
nigrostriatal degeneration when
several people developed typical PD
signs after injecting themselves with a
drug contaminated with MPTP.

Genetics
Although PD is generally an
idiopathic disorder, there is a
minority of cases (10–15%) that
report a family history, and about 5%
have Mendelian inheritance
Autosomal dominant PD
The first type of familial PD caused
by a point mutation in the α-synuclein
gene (SNCA) was discovered in 1997
(44). Four additional point mutations,
as well as gene duplication or
triplication, have now been linked to
autosomal dominant PD

Autosomal recessive PD
Autosomal recessive forms of PD
typically present with an earlier onset
than classical PD. Three of the
PARK-designated genes causing
autosomal recessive PD have been
linked to mitochondrial homeostasis
(PRKN, PINK1, and DJ-1).
 PATHOPHYSIOLOGY: -

Parkinson’s disease is associated with decreased levels of dopamine

resulting from destruction of pigmented neuronal cells in the
substantia nigra in the basal ganglia region of the brain. Fibers or
neuronal pathways project from the substantia nigra to the corpus
striatum, where neurotransmitters are key to the control of complex
body movements. Through the neurotransmitters acetylcholine
(excitatory) and dopamine (inhibitory), striatal neurons relay
messages to the higher motor centers that control and refine motor
movements. The loss of dopamine stores in this area of the brain
results in more excitatory neurotransmitters than inhibitory
neurotransmitters, leading to an imbalance that affects voluntary
movement. Clinical symptoms do not appear until 60% of the
pigmented neurons are lost and the striatal dopamine level is
decreased by 80%. Cellular degeneration impairs the extrapyramidal
tracts that control semiautomatic functions and coordinated
movements; motor cells of the motor cortex and the pyramidal tracts
are not affected. Researchers are working on uncovering the exact
mechanism of neurodegeneration; current theories suggest that it
results from oxidative stress in a portion of the neuron known as
Lewy bodies, protein aggregation, or a combination of the two
mechanisms (Barker & Barasi, 2008).

CLINICAL MANIFESTATIONS: -

BOOK PICTURE PATIENT PICTURE

Parkinson’s disease has a Patient had complaints of;

gradual onset, and symptoms  Mask like appearance
progress slowly over a chronic,  Drooling of saliva
prolonged course. The cardinal  Deformities in legs and hands
signs are tremor, rigidity,  Stooped posture
 Unable to stand
bradykinesia (abnormally slow
 Difficulty in swallowing
movements), and postural  Tremors present in hands
instability.  Bradykinesia present
 Rigidity present
Tremors
Although symptoms are
variable, a slow, unilateral
resting tremor is present in the
majority of patients at the time
of diagnosis. Resting tremor
characteristically disappears
with purposeful movement but is
evident when the extremities are
motionless.
The tremor may manifest as a
rhythmic, slow turning motion
(pronation–supination) of the
forearm and the hand and a
motion of the thumb against the
fingers as if rolling a pill
between the fingers. Tremor is
present while the patient is at
rest; it increases when the patient
is walking, concentration.

Rigidity
Resistance to passive limb
movement characterizes muscle
rigidity. Passive movement of an
extremity may cause the limb to
move in jerky increments,
referred to as lead-pipe or cog-
wheel movements.

Involuntary stiffness of the

passive extremity increases
when another extremity is
engaged in voluntary active
movement. Stiffness of the arms,
legs, face, and posture are
common. Early in the disease,
the patient may complain of
shoulder pain due to rigidity.
Bradykinesia One of the most
common features of Parkinson’s
disease is bradykinesia, which
refers to the overall slowing of
active movement.Patients may
also take longer to complete
activities and have difficulty
initiating movement, such as
rising from a sitting position or
turning in bed.

Postural Instability
The patient commonly develops
postural and gait problems. A
loss of postural reflexes occurs,
and the patient stands with the
head bent forward and walks
with a propulsive gait. The
posture is caused by the forward
flexion of the neck, hips, knees,
and elbows.

The patient may walk faster and

faster, trying to move the feet
forward under the body’s center
of gravity (shuffling gait).
Difficulty in pivoting causes loss
of balance (either forward or
backward). Gait impairment and
postural instability place the
patient at increased risk for falls
Psychiatric changes include
depression, dementia
(progressive mental
deterioration), delirium, and
hallucinations. Depression is
common; whether it is a reaction
to the disorder or is related to a
biochemical abnormality is
uncertain. Mental changes may
appear in the form of cognitive,
perceptual, and memory deficits,
although intellect is not usually
affected.
A number of psychiatric
manifestations (personality
changes, psychosis, dementia,
and acute confusion) are
common in elderly patients with
Parkinson’s disease. Dementia
affects up to 75% of patients
over the course of the disease.

In addition, auditory and visual

hallucinations have been
reported in up to 40% of people
with Parkinson’s disease and
may be associated with
depression, dementia, lack of
sleep, or adverse effects of
medications.

Hypokinesia (abnormally
diminished movement) is also
common and may appear after
the tremor. The freezing
phenomenon refers to a transient
inability to perform active
movement and is thought to be
an extreme form of bradykinesia.
Additionally, the patient tends to
shuffle and exhibits a decreased
arm swing.

As dexterity declines,
micrographia (small
handwriting) develops. The face
becomes increasingly masklike
and expressionless, and the
frequency of blinking decreases.
Dysphonia (soft, slurred, low-
pitched, and less audible speech)
may occur as a result of
weakness and incoordination of
the muscles responsible for
speech.

In many cases, the patient

develops dysphagia, begins to
drool, and is at risk for choking
and aspiration.

DIAGNOSTIC STUDIES: -

BOOK PICTURE PATIENT PICTURE

 History Collection History Collection and physical

 Physical Examination examination was done, X-ray and Ct
 X-ray scan of thorax was done for my
 CT-scan patient
 MRI
 PET scan
 SPECT

MEDICAL MANAGEMENT

BOOK PICTURE PATIENT PICTURE

Although laboratory tests and Patient was earlier diagnosed with

imaging studies are not helpful to the Parkinson’s disease since 10 years
clinician in diagnosing Parkinson’s back.
disease, ongoing research with PET
and single photon emission computed
tomography (SPECT) scanning has
been helpful in understanding the
disease and advancing treatment.
Currently, the disease is diagnosed
clinically from the patient’s history
and the presence of two of the four
cardinal manifestations: tremor,
rigidity, bradykinesia, and postural
changes. Early diagnosis can be
difficult because patients rarely are
able to pinpoint when the symptoms
started. Often, a family member
notices a change such as stooped
posture, a stiff arm, a slight limp,
tremor, or slow, small handwriting.
The medical history, presenting
symptoms, neurologic examination,
and response to pharmacologic
management are carefully evaluated
when making the diagnosis.

PHARMACOLOGIC THERAPY
Antiparkinsonian medications act by
(1) increasing striatal dopaminergic
activity; (2) reducing the excessive
influence of excitatory cholinergic
neurons on the extrapyramidal tract,
thereby restoring a balance between
dopaminergic and cholinergic
activities; or (3) acting on
neurotransmitter pathways other than
the dopaminergic pathway. Levodopa
(Larodopa) is the most effective agent
and the mainstay of treatment.

Levodopa is converted to dopamine

in the basal ganglia, producing
symptom relief. Levodopa is
available in three forms: immediate-
release, orally disintegrating, and
sustained-release tablets (Halkias,
Haq, Huang, et al., 2007). The
beneficial effects of levodopa are
most pronounced in the first few
years of treatment. Benefits begin to
wane and adverse effects become
more severe over time.
Confusion, hallucinations, depression,
and sleep alterations are associated
with prolonged use. Within 5 to 10
years, most patients develop a
response to the medication
characterized by dyskinesia
(abnormal involuntary movements),
including facial grimacing, rhythmic
jerking movements of the hands, head
bobbing, chewing and smacking
movements, and involuntary
movements of the trunk and
extremities.

The patient may experience and on–

off syndrome in which sudden
periods of near immobility (“off
effect”) are followed by a sudden
return of effectiveness of the
medication.

SURGICAL MANAGEMENT
BOOK PICTURE PATIENT PICTURE
The limitations of levodopa therapy, Patient did not went for any surgical
improvements in stereotactic surgery, procedure
and new approaches in
transplantation have renewed interest
in the surgical treatment of
Parkinson’s disease. In patients with
disabling tremor, rigidity, or severe
levodopa-induced dyskinesia, surgery
may be considered. Although surgery
provides symptom relief in selected
patients, it has not been shown to
alter the course of the disease or to
produce permanent improvement.

Stereotactic Procedures
Thalamotomy and pallidotomy are
effective in relieving many of the
symptoms of Parkinson’s disease.
Patients eligible for these procedures
are those who have had an inadequate
response to medical therapy; they
must meet strict criteria to be eligible.

Candidates eligible for these

procedures are patients with
idiopathic Parkinson’s disease who
are taking maximum doses of
antiparkinsonian medications.
Patients with dementia and atypical

Parkinson’s disease are usually not

considered for stereotactic
procedures. Parkinson’s disease
rating scales and specific neurologic
tests are used to identify eligible
patients. The intent of thalamotomy
and pallidotomy is to interrupt the
nerve pathways and thereby alleviate
tremor or rigidity.

During thalamotomy, a stereotactic

electrical stimulator destroys part of
the ventrolateral portion of the
thalamus in an attempt to reduce
tremor; the most common
complications are ataxia and
hemiparesis. Pallidotomy involves
destruction of part of the ventral
aspect of the medial globus
pallidus through electrical stimulation
in patients with advanced disease.

The procedure is effective in reducing

rigidity, bradykinesia, and dyskinesia,
thus improving motor function and
ADLs in the immediate postoperative
course. Potential complications
include hemiparesis and stroke, as
well as cognitive, speech,
swallowing, and visual changes.
A CT scan, x-ray, MRI scan, or
angiogram is used to localize the
appropriate surgical site in the brain.
Then the patient’s head is positioned
in a stereotactic frame. After the
surgeon makes an incision in the skin
and a burr hole, an electrode is passed
through to the target area in the
thalamus or globus pallidum.
The desired response of the patient to
the electrical stimulation (ie, a
decrease in rigidity) is the basis for
the selection of the area of the brain
to be destroyed. Stereotactic
procedures are completed on one side
of the brain at a time. If rigidity or
tremor is bilateral, a 6-month interval
is suggested between procedures.
Neural Transplantation Ongoing
research is exploring transplantation
of porcine neuronal cells, human fetal
cells, and stem cells (Rowland, 2005).
Legal, ethical, and political concerns
surrounding the use of fetal brain
cells and stem cells have limited the
implementation of these procedures.

Deep Brain Stimulation

Pacemakerlike brain implants are
used to relieve tremors (Rowland,
2005). The stimulation can be
bilateral or unilateral; bilateral
stimulation of the subthalamic
nucleus is thought to be of greater
benefit to patients than results
achieved with thalamotomy,
pallidotomy, or fetal nigral
transplantation.
In deep brain stimulation, an
electrode is placed in the thalamus
and connected to a pulse generator
that is implanted in a subcutaneous
subclavicular or abdominal pouch.
The battery-powered pulse generator
sends high-frequency electrical
impulses through a wire placed under
the skin to a lead anchored to the
skull. The electrode blocks nerve
pathways in the brain that cause
tremors. These devices are not
without complications that can result
from both the surgical procedure
needed for implantation and the
device itself (eg, lead leakage)
 LIST OF NURSING DIAGNOSIS
1) Ineffective airway clearance related to Parkinsonian changes in
musculature and bronchospasm as evidenced by increased breathing
effort and use of accessory muscles.
2) Impaired verbal communication related to physical barrier from
hypertonicity from Parkinsonism as evidenced by inability to speak.
3) Impaired physical mobility related to Parkinson’s disease as evidenced by
balance and coordination deficits.
4) Impaired swallowing related to Parkinson’s disease as evidenced by
inability to swallow effectively.
5) Disturbed thought process related to parkinsonian medications as
evidenced by inability to perform activities as before.
6) Ineffective coping related to progressive chronic disease as evidenced by
inappropriate coping strategies
7) Deficient knowledge related to cognitive impairment as evidenced by
inability to follow instructions
8) Risk for injury related to Parkinson’s disease and loss of awareness
related to environmental hazards

DIET EDUCATION
Antioxidants

Current research focuses on proteins. Trusted Source, flavonoids, and gut bacteria.
Trusted Source for improving Parkinson’s symptoms. In the meantime, eating a
diet high in antioxidants reduces “oxidative stress” that aggravates Parkinson’s and
similar conditions, according to the Michael J. Fox Foundation for Parkinson’s
research.

You can get lots of antioxidants by eating:

 tree nuts, like walnuts, Brazil nuts, pecans, and pistachios

 blueberries, blackberries, goji berries, cranberries, and elderberries
 tomatoes, peppers, eggplant, and other nightshade vegetables
 spinach and kale

Eating a plant-based diet high in these types of foods may provide the highest
antioxidant intake.
Clinical trials over the last decade explored the idea of antioxidant treatment for
Parkinson’s, but these trials didn’t find concrete evidence to link antioxidants to
Parkinson’s treatment. But decreasing oxidative stress is still a simple way to
improve your lifestyle and get healthier. In other words, it can’t hurt.

Fava beans

Some people eat fava beans for Parkinson’s because they contain levodopa — the
same ingredient in some drugs used to treat Parkinson’s. There’s no definitive
evidence supporting fava beans as a treatment at this time. Since you don’t know
how much levodopa you’re getting when you eat fava beans, they can’t substitute
for prescription treatments.

Omega-3s

If you’re concerned about secondary symptoms of Parkinson’s, like dementia and

confusion, get serious about consuming more salmon, halibut, oysters, soybeans,
flax seed, and kidney beans. SoyTrusted Source in particular is being studied for its
ability to protect against Parkinson’s. These foods contain omega-3 fatty acids,
which might improveTrusted Source cognitive function.

Other tips
 For constipation caused by Parkinson’s, try seasoning your food with
turmeric or yellow mustard to encourage bowel movements.
 One study suggestedTrusted Source that consuming caffeine might help
slow down the progression of Parkinson’s.
 For muscle cramps caused by Parkinson’s, consider drinking tonic water for
the quinine it contains or upping your magnesium through diet, Epsom salt
baths, or supplements.
Foods to avoid
Dairy products

Dairy products have been linkedTrusted Source to a risk of developing

Parkinson’s. Something in dairy products might negatively impact the oxidation
levels in your brain, making symptoms more persistent. This effect was shown to
be stronger in men than in women and not seen in those supplementing with
calcium.

If you’re going to stop consuming dairy products like milk, cheese, and yogurt,
you might want to consider a calcium supplement to make up for the loss of
calcium in your diet. However, low calcium intake doesn’t necessarily equal poor
bone health, as seen in countries with low dairy and calcium consumption.

Recent research suggests that a defect in how the body manages calcium ions
(Ca2+), the form of calcium residing in bone, and also present in dairy, might be to
blame for the progression of Parkinson’s disease.

Foods high in saturated fat

The role that foods high in saturated fats play in Parkinson’s progression is still
under investigationTrusted Source and is often conflicting. We might eventually
discover that there are certain types of saturated fats that actually help people with
Parkinson’s.

Some limited research does show that ketogenic, low-protein diets were beneficial
for some with Parkinson’s. Other research finds high saturated fat intake worsened
risk.

But in general, foods that have been fried or heavily processed alter your
metabolism, increase blood pressure, and impact your cholesterol. None of those
things are good for your body, especially if you’re trying to treat Parkinson’s.
HEALTH EDUCATION FOR PARKINSON’S
DISEASE

COVID-19 AND PARKINSON DISEASE

COVID-19 stands for "coronavirus disease 2019." It is an infection caused by a

virus called SARS-CoV-2. The virus first appeared in late 2019 and has since
spread throughout the world. People in many areas have been told to stay home
as much as possible in order to slow the spread of the virus. Especially at the
beginning of the pandemic, and while the virus was spreading quickly in a lot of
places, people in many areas were told to stay home as much as possible in
order to slow the spread. This has been particularly important for older adults,
as they are at increased risk of severe illness if they get COVID-19. However,
for people with PD, this risk must be balanced against the importance of
continuing to get regular medical care.

If you live in an area where there are still lots of cases of COVID-19, your
doctor can talk to you about whether you should make any changes to your
usual treatment plan or schedule. In some cases, it may be an option to reduce
the number of appointments you need to attend in person. This will depend on
several different things, including where you live, how much the virus is still
spreading in your community, which therapies you currently receive, and your
overall health.

PARKINSON DISEASE EDUCATION

Being diagnosed with a chronic disease can be a frightening experience, filled

with uncertainty about what the future holds. This is especially true if the person
knows a friend or family member who has experienced the disabling effects of
Parkinson disease.

In the first months and years after being diagnosed with Parkinson disease, it is
important to gather information about initial symptoms and the treatment
options that are available.
 PARKINSON DISEASE SUPPORT

A person may respond to the diagnosis of Parkinson disease with anger, fear,
depression, anxiety, resentment, or a combination of these emotions. Concerns
about social and financial well-being are common. Support groups can help the
patient and family to interact with other individuals who have the same
diagnosis to allow these people to share experiences and information.

People with young-onset Parkinson disease may benefit from a group composed
of similar-aged patients.
Other types of support are available for people with Parkinson disease and their
families, including psychologic, financial, legal, or occupational counseling. A
physician, nurse, or social worker can usually provide contact information for
these services in the local area.

EXERCISE AND PHYSICAL THERAPY

Many studies suggest that exercise may slow the progression of Parkinson
disease. However, this will have to be confirmed by prospective clinical trials to
document this effect on disease progression.

Exercise can also help patients feel better, both physically and mentally.
Aerobic exercise may have a positive effect on disease status while improving
quality of life and socialization. Favorable studies have appeared in the medical
literature on exercises to improve balance, flexibility, and strength (including
dance and tai chi). However, these reports will need to be confirmed in larger
groups of people followed for longer periods of time.

Exercise can help to prevent some of the complications of Parkinson disease

caused by rigidity and flexed (or bent) posture, such as shoulder, hip, and back
pain. The benefits of exercise will persist as long as exercise continues.

Many patients who participate in an exercise program feel more confident and
gain a sense of control over their disease. Parkinson-specific exercise programs
also provide a source of social support and camaraderie, separate from and
complementary to the support options above.

Simple strengthening and stretching exercises are important for everyone with
Parkinson disease. Aerobic exercises, such as walking (outdoors or on a
treadmill, with support), riding a stationary bicycle, swimming, or water
aerobics, are easy to perform and usually energizing. A physical therapist can
help you develop an exercise program that suits your needs.

PARKINSON DISEASE SAFETY ISSUES

Falls prevention — As Parkinson disease gets worse, the risk of falling

increases. To reduce this risk, patients and caretakers are encouraged to make
the home as safe as possible by:
●Installing shower or tub grab-bars, nonslip tape on floors, and elevated
toilet seats with handles.
●Having adequate lighting in the house, especially at night. Use of light-
sensitive night lights or lamps on a timer may be helpful.
●Securing loose rugs, which can increase the risk of tripping.

Driving safety — Most people with Parkinson disease can continue to drive as
long as their motor symptoms remain mild. Driving ability must be monitored
and formally re-evaluated if and when motor and cognitive symptoms worsen.
The Association for Driver Rehabilitation Specialists can provide names of
local occupational therapists or driving specialists who can perform driving tests
to see if Parkinson disease is affecting driving, and neurologists can provide
referrals for these evaluations.
If it is necessary to stop or cut back on driving, other forms of transportation are
available, such as taxi cabs, shuttle buses, public buses, or trains. Walking, if
practical, is always a healthy way to get around. The Eldercare Locator is a
resource that can provide assistance in locating help with transportation as well
as housing, financial or legal services, health insurance, and long-term care.

PARKINSON DISEASE SPEECH THERAPY

Problems with speech, including slurred speech and speaking too quietly, are
common in people with Parkinson disease. These problems develop as muscles
weaken in the voice box, throat, mouth, tongue, and lips.

A voice or speech therapist can help overcome speech problems. This may
involve training to speak more loudly and clearly, conserving energy when
speaking (speaking only important words and phrases), and using nonverbal
methods such as a letter or word board, or hand signals.
A speech therapist can also evaluate and treat problems with swallowing. The
medical term for difficulty with swallowing is "dysphagia." Dysphagia can
increase the risk of coughing, choking, or inhaling food (aspiration), which can
lead to pneumonia. Treatments for dysphagia may include sitting up straight
while eating, tilting the head slightly forward, eating small bites and chewing
completely, and not speaking while eating. Another treatment is the use of a
powder to thicken liquids or thin food, making them easier to swallow.

PARKINSON DISEASE NUTRITION

There is no specific diet recommended for people with Parkinson disease.

Several studies suggest that the MIND diet (Mediterranean-DASH Intervention
for Neurodegenerative Delay) reduces the risk of dementia in people at risk for
or with early signs of Parkinson disease, and reduces the risk of Alzheimer
disease.

Some patients notice that protein in a meal can block the effect of a dose of
levodopa taken around meal time. People who notice this effect should speak to
their healthcare provider about adjusting the timing of their medications, rather
than simply avoiding protein, which can lead to loss of muscle mass.

It is important to be sure that the person is getting an adequate number of

calories and nutrients to maintain strength, bone structure, and muscle mass.
Problems with unintended weight loss, poor appetite, eating and swallowing, or
preparing food should be discussed with a healthcare provider. The provider
may recommend meeting with a registered dietitian.
 SUMMARY
Parkinson's disease (PD) is a type of movement disorder. It happens when
nerve cells in the brain don't produce enough of a brain chemical called
dopamine. Sometimes it is genetic, but most cases do not seem to run in
families. Exposure to chemicals in the environment might play a role.
Symptoms begin gradually, often on one side of the body. Later they affect both
sides. They include:

 Trembling of hands, arms, legs, jaw and face

 Stiffness of the arms, legs and trunk
 Slowness of movement
 Poor balance and coordination
As symptoms get worse, people with the disease may have trouble walking,
talking, or doing simple tasks. They may also have problems such as
depression, sleep problems, or trouble chewing, swallowing, or speaking. There
is no specific test for PD, so it can be difficult to diagnose. Doctors use a
medical history and a neurological examination to diagnose it. PD usually
begins around age 60, but it can start earlier. It is more common in men than in
women. There is no cure for PD. A variety of medicines sometimes help
symptoms dramatically. Surgery and deep brain stimulation (DBS) can help
severe cases. With DBS, electrodes are surgically implanted in the brain. They
send electrical pulses to stimulate the parts of the brain that control movement.
 CONCLUSION
Parkinson’s disease is no longer considered just a motor
disorder. There is a prolonged pre-motor component. There are
clinical criteria for the diagnosis of the motor component. Parkinson’s
disease continues to be a clinical diagnosis. Diagnostic tools are
supportive. Research suggests that Parkinson’s disease affects
500,000 people in the United States each year. My patient had
Parkinson since many years she was having iron-deficiency anemia
with that problem and the condition worsened. But the family was
cooperative and understood about the disease condition and took good
care of the patient.
BIBLIOGRAPHY