Extra pyramidal system

1. Striato pallidonigral pathway (Basal ganglia)

2. Cerebellum

Anatomy Part -1 -Basal ganglia

• Form a group of subcortical nuclei situated in the proximity of Thalamus and
Hypothalamus.

• Main structures are striatum,pallidum, substantia nigra pars compacta and

reticulata, and subthalamic nucleus.

• These regions connect to cortex and spinal cord and modulate motor and
cognitive functions.
Nucleus accumbens
• Linked to mesolimbic dopaminergic Reward system
• Situatated between caudate and putamen in basal fore brain .part of ventral
striatum.
• Contains Dopamine .
• Important for motivation.
Extra pyramidal tracts.
[Link] by fibers arising from the motor cortex, Which do not enter the
pyramidal tracts.

2. They relay in the various parts of the brain:-

basal ganglia. Red nucleus, reticular formation of brain stem and vestibular
nuclei, and consitute a multisynaptic pathway controlling the contralateral side.

3. Functions: concerned with regulation of muscle tone, posture and equilibrium.

Basal ganglia function
■ Selecting appropriate motor or behavioral output in a particular context
■ Strong convergence of corticostriatal projections
■ Topographical arrangements
■ Dorsolateral sensorimotor
■ Central associative
■ Ventral limbic
■? Exact neural structure for selection process

Components of somatic motor control system (1)

Three tier system:
1. Highest level of motor control. cerebral cortex-motor areas.

[Link] level of motor control.

sub-cortical centers-basal ganglia, cerebellum and brain stem nuclei.

[Link] level of motor control. cranial nerve nuclei in brain stem, spinal cord.

Components of somatic motor control system(2)

1.. Primary motor cortex area 4. Initiation of voluntary movements

[Link] area/cortex area [Link] the voluntary activity.

• Co-ordinates the voluntary action of area-4 and extra pyramidal system.

• Assist Intergratation of sensory motor information & Smooth and accurate

skilled movements (Praxis).

3. Supplementary motor cortex (area 6).

In medial surface of frontal lobe rostral to primary area.
Responsible for generating the idea, planning and programming of movements,
with basal ganglia and [Link] ipsilateral & contralateral based on
remembered sequence of movements.

It needs simultaneous input from SN &Cortex. Integrates inputs even

subthreshold ones [Link].

4. area-8. Frontal eye field. Concerned with control of eye movements

Sensory system in motor control?

• Positive cortical tropism
• Phenomena of agency

Input and output of the basal ganglia

• The caudate nucleus and the putamen form the main sites for receiving input to
the basal nuclei.

• The globus pallidus forms the major site from which the output leaves the basal
nuclei.

• They receive no direct input from or output to the spinal cord.

Functions of the pathways

• To facilitate desired movement

• To inhibit unwanted movements (Movement brake)

• To provide feedback mechanism and correction of erroneous movements

• Direct pathway selectively facilitates certain motor (or cognitive) programs in

the cerebral cortex that are adaptive for the present task

• Indirect pathway simultaneously inhibits the execution of competing motor

programs

• Hyperdirect pathway is critical for suppressing erroneous movement

Five cortico-BG-thalamo-cortical loops(Closed loops)
• 1) motor. (De Long)
• 2) oculomotor.
• 3) associative.
• 4) limbic.
• 5) orbitofrontal.

• In addition, the BG are intimately interconnected with brain stem nuclei such as
the locus ceruleus (noradrenergic), raphe nuclei (serotonergic) and cholinergic
the reticular formation.
Functions of the subcortical circuits
• 3. dorsolateral prefrontal . Executive functions: motor planning, organisation,
deciding which stimuli to attend to, shifting cognitive sets, sequencing, Attention
span and working memory.

• 4. Anterior Cingulate. Motivated behaviour, Impaired motivation, akinetic

mutism, apathy, poverty of speech, poor response inhibition

• [Link] orbitofrontal. Emotional life, personality structure, social response,

judgement, Arousal, motivation, affect, Emotional incontinence, irritability, undue
familiarity, OCD, mood disorders

basal ganglia control of movements

• [Link] networks
• [Link] motor networks
• Particular patterns of movements such as saccade, mastication, vocalisation,
swallowing, locomotion thought to be generated by specific neuronal networks in
the brainstem and spinal cord

Specific Neurotransmitter Substances in the Basal Ganglia System

(1) dopamine pathways from the substantia nigra to the caudate nucleus and
putamen

(2) gamma-aminobutyric acid (GABA) pathways from the caudate nucleus and
putamen to the globus pallidus and substantia nigra

(3) acetylcholine pathways from the cortex to the caudate nucleus and putamen

(4) multiple general pathways from the brain stem that secrete norepinephrine,
serotonin, enkephalin

Symptoms of basal ganglia disease

• Altered tone
• Altered speed
• Altered posture & movements
• Praxis
• Impaired voluntary control
• Abnormal movements

Akinesia, Bradykinesia,Hypokinesia, Bradyphrenia

Hypo kinesia: indicates decreased amplitude of movement -paucity of movement

in the absence of weakness or paralysis.

• Bradykinesia decreased speed of movement.

• Akinesia is absence of movement.

• Brady phrenia -mental slowing in the absence of dementia

• All in the Absence of paralysis

Alteration in voluntary movements

• Hastening ----- enhancement -festination
• Freezing ----inhibition

Tone & Rigidity .

• Tone: Tension in the relaxed muscles due to involuntary contraction of motor

units.

• Resistance to passive movements.

• State of partial contraction always present in normal muscle for maintenance

of posture with minimal expenditure of energy.

• [Link] resistance to passive movement which affects both agonist and

antagonist and constant through out the entire range of movement.

• Cogwheel rigidity; periodic modification of rigidity by associated tremor which

is appreciated during passive movements.

Abnormal movements-approach
• Hypokinetic --- Bradykinesia, Athetosis, Dystonia
• Hyperkinetic -Tremor, Tic, Myoclonus, Chorea, Ballismus, asterixis
• Mixed

What next
• The phenomenology-describe rate, range, rhythm, direction ,amplitude, what
happens in sleep, emotional states, drugs &alcohol, any gesta antogonistica ?
• What is the anatomy
• What pathology/syndrome
• Treatment plan

Tremor
• Involuntary and rhythmic oscillatory movement around a fixed point produced
by alternating or irregularly synchronous contractions of reciprocally innervated
muscles. (tremor loop)

Rest tremor:
Tremor in a body part that is completely supported and resting

Action tremor:
Tremor occurring during voluntary actions

Postural:
When a body part is voluntarily maintained against gravity

Kinetic:
During guided voluntary movement

Simple kinetic
Intention tremor:
increasing amplitude during pursuit of a target

Isometric tremor:
Evoked by voluntary muscle contractions without movement

Task-specific tremors:
• Primary Writing Tremor-Pronation-supination tremor
• Elicited by pronation of forearm during writing

• Type A: appears during the act of writing

• Type B: When the position for writing is adopted

Musicians
Golfers

Intention tremor
• Occurs during the most demanding part of active movement
• exacting, precise, and projected movement
• Irregular, proximal, more or less rhythmic (2-3 Hz) movement in > one plan

Orthostatic tremor
• Mainly affects legs and trunk
• Presents on standing
• Leg cramps- tetanic contractions of calf muscles
• Palpate the muscle
• Thigh/calf auscultation: thumping sound
• Electrophysiology-Rapid: 14-16 Hz

Chorea
• Quasive purposive, non repetitive,jerky, distal movements
• Limbs/ grimacing/peculiar respiratory sounds
• Excessively quick and poorly sustained voluntary movements
• Hypotonia, pendular knee-jerks, hung-up reflex
• Milkmaid sign, lizard tongue, quick pronator sign
• Can be unilateral (hemichorea)
• Caudate

Ballism
• Violent swinging movements proximal & distal
• Persists in sleep
• Subthalamic nucleus

Myoclonus
• Sudden shock like contraction of a single muscle, group of muscles, or whole
person
• Epileptic or non epileptic
• Cortical, subcortical and spinal

Tics
• Compulsive
Repetitive, Voluntarily controllable but build-up" Eventually "rebound
⚫ sudden, abrupt, unpredicatable, brief, (clonic tics), or less commonly the
movements are more sustained and patterned (dystonic or tonic tics)
• Can persist in sleep

Hypokinetic-Athetosis
• Inability to sustain the fingers, toes, tongue, or any part of the body in one
position
• Posture interrupted by slow, sinuous, purposeless movements, which have a
tendency to flow into one another
• Striatum

Dystonia
• A syndrome dominated by sustained muscle contractions, frequently causing
twisting and repetitive movements, or abnormal postures
• Peak of the movement is stationary for 30 seconds to 1 minute

Classification
1. By cause
(a) Idiopathic
Sporadic

Familial
(b) Symptomatic

2. By age at onset
(a) Childhood-onset: 0-12 years
(b) Adolescent-onset: 13-20 years
(c) Adult-onset: > 20 years

3. By distribution
(a) Focal
(b) Segmental
(c) Multifocal
(d) Generalized
(e) Hemidystonia

• By association
• Primary dystonia
• Dystonia plus
• Dystonia as part of heredodegenerative disorders
•Paroxysmal dystonia
• Drug related

Posture & Equilibrium &Movement

• Posture :Ability to maintain body parts in desired alignment in balance with
gravitational pull. (postural reflexes replace the primitive reflexes.)

• Equilibrium :Stable maintenance of Posture during rest and activity

• Movement:Ability of the organism to displace from one plane to another.
• It involves short phasic reactions mediated through several reflexes.
# Postural and righting reflexes
# Antigravity stretches
# Stepping
# Equilibrium
# Propulsion
Gait, Praxis, Righting reflexes
• Gait .learned motor skill which is the most automatic of all automatic reflexes
in which the erect moving body is first supported on one leg and then the other.

• [Link] to formulate skilled movements in a non paretic limb on

command based on stored complex information and previously learned
movements.

• Righting reflexes' Coordinated synergies that help to bring the head

and body in to upright position during stance and locomotion.

• Visual, vestibular, proprioceptive error signals are matched with expected body
posture to correct the difference.

PD- kampa vada of charaka

• Parkinson's Disease is a slowly progressive, neuro-degenerative disorder

• In the early stage the motor symptoms predominate but over years the disease
progresses with appearance of treatment related motor fluctuations, dyskinesias
and many non motor symptoms.

• "Involuntary tremulous motion, with lessened muscular power, in parts not in

action and even when supported; with a propensity to bend the trunk forward,
and to pass from a walking to a running pace, the senses and intellect being
uninjured." James parkinsan

Parkinsonism
TRAP
Tremor
Rigidity
Akinesia
Postural instability

Diagnosis of Parkinson's Disease

UK Parkinson's Disease Society
Brain Bank Criteria
Step 1
• 1. Bradykinesia
AND
2. At least one of the following:
• Muscular rigidity
• 4-6 Hz rest tremor
• Postural instability

Diagnosis of Parkinson's Disease

UK Parkinson's Disease Society Brain Bank Criteria

Step 3: Supportive Prospective Criteria

(Three or more needed for +ve diagnosis
• Unilateral onset
• Rest tremor present
• Progressive disorder
• Persistent Asymmetry with side of onset most excellent response to levodopa
(70-100%)
• Severe levodopa-induced chorea
• Persistent levodopa benefit for > 5 years
• Clinical course of > 10 years

Parkinson-Plus Syndrome
Parkinsonism + other neurological signs
• Supranuclear Gaze Palsy:
• PSP
• CBGD
• Autonomic failure: Multiple System Atrophy (MSA)
• Apraxia: Cortico-Basal ganglionic degeneration (CBGD)
• Cerebellar Signs:
• MSA
• CJD

Parkinson-Plus Syndrome
Parkinsonism + other neurological signs
• Dementia:
• Diffuse Lewy Body disease
• PD+AD, CBGD
• Juvenile Huntington's Disease
• (NBIA). Hallervorden Spatz disease

Secondary Parkinsonism

Parkinsonism secondary to a known etiological agent

• Neuroleptics
• Toxins: Manganese, Pesticides, MPTP
• Metabolic: Wilson's disease, Hypo/hyper parathyroidism
• Tumor
• Normal Pressure hydrocephalus
• Head injury: Dementia Puglistica
• Multiple Infarctions
• Psychogenic

Akinetic Rigid syndromes

Akinetic rigid syndrome implies slowness of initiation generally involving upper
body more than lower (akinesia)and rigidity characterized by abnormal stiffness
due to increase in tone of both the agonist and antagonist (lead pipe) or
cogwheel.

Diagnosis is clinical
Bradykinesia, brady phrenia, hypokinesia,postural instability and tremors also
accompany

Classification of Akineto-rigid syndromes

• [Link]- parkinsons disease & cortico basal syndromes

• [Link]- PSP & MSA

• [Link] -vascular, metabolic, traumatic, toxic, DLBD, etc

Primary Causes of Atypical Parkinsonism

Multisystem Disease
• Progressive supranuclear palsy
• Corticobasal syndrome
• Multiple system atrophy
• Dementia with Lewy bodies
• Parkinsonism-dementia-amyotrophic lateral sclerosis
Nikolaus R et al, 2016

Heredodegenerative Disorders
• Huntington disease
• Spinocerebellar ataxias (especially types 2, 3, and 17)
• Wilson disease
• Hereditary ceruloplasmin deficiency
• Neuronal brain iron accumulation disorders (eg, PKAN2)
• X-linked dystonia-parkinsonism (Lubag disease)
• Gerstmann-Straussler-Scheinker syndrome
• Neuronal ceroid lipofuscinoses
• Mitochondrial cytopathies

Components
• 1. bradykinesia
• [Link]
• [Link] signs &speech
• [Link] features
• [Link]
• [Link] and postural reflexes
• [Link], dystonia, tremor

Factors involved in gait

• Postural and Righting reflexes
• Integration and initiation – Cortico spinal
• Automatic movements - Extra pyramidal system
• Coordination – Cerebellar
• Subjective awareness - Proprioceptive

Skilled purposeful movements

• During skilled movements posture control integrates different neural systems
including cognition.

• They are broadly egocentric (Body), Exocentric (environment),

Gravity(geocentric).

• The needs are 1. Alighnment of body parts for erect stance.

• [Link] for voluntary movements.
• [Link] dynamics like situations like dance.
• [Link] do at minimum energy demand
Freezing
• Brief episodes of inability to initiate or continue locomotion

• Happens during change or stress.

• Happens at initiation, during locomotion or during testing circumstances .

• Response motor or behavioural tricks

What is a fall ?
• A fall was defined as “an unexpected event in which the person comes to rest
on the ground, floor, or lower level not due to a seizure or an acute stroke.

• Fall calendar is documentation of the event, the circumstances, and

characteristics of the fall.

• Multiple falls was defined as having at least two falls or more during the follow-
up period.

• Injurious falls was defined as falls that provoked visible skin damage, including
lacerations, bruises, joint injuries(eg, inflammation, swollen, or separation),
fractures, and/orhead trauma.
Fall Syndromes
1. Collapsing
a. Akinetic seizures
b. Syncope
c. Orthostatic hypotension

2. Toppling
a. while standing
b. while changing position/posture

3. Tripping
4. Freezing
5. Non-patterned
Falls in the current scenario
• Idipathic PD - En block turning-fall-righting reflexes
• CBD - postural
• PSP- Pivotal falls -Oscillators abnormality
• MSA- postural-Autonomic
• DLBD- syncope - carotid body increased baroreceptor sensitivity

• Falls, Freezing & REM sleep behavioural disorder are linked to changes in
mesencephalic reticular formation, balance centre PPN&Locus Coeruleus.

• Dopamine improves steplength &speed but vertical breaking ability needed to

improve falls does not change. As it is cortical & PPN cholinergic denervation
that causes falls.

Depression and Apathy in PD

• Indirect pathway activity ↑

• Direct pathway activity↓

• Inhibition of thalamocortical neurons ↑

• 20% patients present with severe depression in advanced PD.

• Dysfunction of subcortical nuclei and prefrontal cortex (PFC), striatal-thalamic-

PFC circuits and the basotemporal limbic circuits.

• Anxiety is associated with depression in over 2/3rds of cases and alone in 43%.

• Locus coeruleus dysfunction with reduced noradrenaline has been implicated.

Autonomic Dysfunction in PD
• Lewy bodies are widespread throughout the autonomic nervous system.

• Many autonomic symptoms serve as pre-motor markers.

• Anosmia, constipation, RBD, cardiac sympathetic denervation, bladder

disturbances, erectile dysfunction, Gl distubances and orthostatic hypotension.

Sleep Disturbances in PD

• Sleep disturbances are very common and can affect more than 80%.

• Insomnias, parasomnias and excessive daytime sleepiness (EDS).

• Sleep fragmentation is the most consistent and often the earliest sleep
disturbance
• Exact mechanisms are not known, however levels of neurotransmitters that
mediate sleep functions (norepinephrine, serotonin, dopamine and GABA) are
altered

GI Disturbances in PD
• Can manifest as weight loss, excessive salivation, drooling, dysphagia,
esophageal dysmotility, gastroparesis and constipation.

• >70% of PD patients experience excessive salivation that can lead to aspiration.

• Esophageal dysmotility (10-80%) with repetitive proximal esophageal

contractions, slowed esophageal transit, aperistalsis and achalasia.

• Constipation - Slowed colonic transit - >50%

Gait Disturbances in PD

• Freezing and falls are difficult to handle in Advanced PD.

• FOG is a heterogeneous symptom that can be divided into dopaminergic-

sensitive, dopaminergic-resistant, and dopaminergic drug-provoked categories.

• usually occurs as a sudden inability to step forward while walking, which may
occur at the beginning ("start hesitation"), at a turn, or just before reaching the
destination leading to falls.

Progressive Supranuclear Palsy

• Most common form of atypical parkinsonism

• Average age of onset - in the sixties (average age of 63 to 66 years)

• The mean survival from diagnosis- 5 to 8 years

Postural Instability & EP Features
• Falls-backward
• Poor postural reflexe
• Rigidity-axial
• Dysarthria-spastic,
• Hypophoni
• ataxic
• Frontal release signs
• Pseudobulbar palsy
• L-DOPA UNRESPONSIVENESS

Clinical Features
• Reduced blink rate and closure of eyelids due to eyelid dystonia or levator
inhibition (apraxia of eyelid opening)
• square wave-jerks
• on doll's eye maneuver, there is improved range, as vestibulo-ocular reflex is
preserved
• Subcortical-type dementia
• Typical facies- "surprised look"

Pathophysiology
• Tauopathy-4-repeat t, 4R tauopathy).
• always sporadic, few familial cases-
• MAPT (microtubuli associated protein t) gene mtn.
• Mitochondrial dysfunction & oxidative stress - pathophysiology of PSP

Variants of PSP
• Five phenotypic variants earlier described were

• PSP-parkinsonism

• PSP-pure akinesia with gait freezing

• PSP-corticobasal syndrome (PSP-CBS) (or primary nonfluent aphasia),

• PSP-behavioral variant of frontotemporal dementia (FTD)

• Two other possible PSP variants with features that overlap with either primary
lateral sclerosis (PLS) or cerebellar ataxia

Nikolaus R et al,2016
Multi system atrophy
■ Multiple system atrophy (MSA) is an adult onset, sporadic, neurodegenerative
disorder characterized

✓ Clinically by a variable combination of parkinsonism, autonomic dysfunction,

cerebellar dysfunction and pyramidal tract involvement, in general with a poor
response to dopaminergic medication (MSA-P,MSA-C)

1. Pathologically by cell loss, gliosis, and abnormal alpha synuclein cytoplasmic

inclusions in several CNS structures (Oligodendroglia and neurons

MSA - P
• Progressive akinesia and rigidity
• jerky postural tremor and tremor at rest.
• orofacial or craniocervical dystonia associated with a characteristic quivering
high-pitched dysarthria.

• Postural stability is compromised early on in the disease course

• Recurrent falls at disease onset are unusual in contrast to psp.

• 90% of the MSA-P pts- unresponsive to levodopa in the long term.

• 50% have levodopa-induced dyskinesia affecting orofacial and neck muscles,

without motor benefit.

• Fully developed clinical picture of MSA-P evolves within 5 years of disease

onset, allowing a clinical diagnosis during follow-up.

MSA - P
• Early instability
• Rapid progression
• Pisa syndrome, camptocormia, contractures
• Bulbar dysfunction
• Respiratory dysfn- stridor,insp sighs
• Emotional incontinence
• 2/6 - probable MSA-P – additional criteria

MSA - C
• gait ataxia
• limb kinetic ataxia
• scanning dysarthria,
• cerebellar oculomotor disturbances.
• Most patients develop additional non-cerebellar symptoms and signs
• may be indistinguishable from other patients with idiopathic late onset
cerebellar ataxia (ILOCA)

Dysautonomia in MSA
• urogenital and orthostatic dysfunction.

• Early erectile dysfunction is nearly universal in men with MSA

• Female- genital insensitivity

• urinary incontinence or retention are common early in the course or as

presenting symptoms

Differentiating Multiple System Atrophy-Parkinsonian Type from Idiopathic

Parkinson Disease

Multiple System Atrophy-Parkinsonian Type (MSA-P)

• Symmetrical onset
• Rapid progression
• Tremor (distal, myoclonic)
• Frequent rigidity, hypokinesia
• Dystonia (axial), anterocollis (dropped head)
• Early falls
• Dysarthria, dysphonia
• Sleep apnea, rapid eye movement (REM) sleep behavior disorder
• Respiratory/laryngeal stridor
• Hyperreflexia, Babinski signs
• Dysautonomia (69% versus 5% in Parkinson disease)
• Poor/unsustained levodopa response (~30%)
Dyskinesia (orofacial common)

Cortico basal syndrome

• The classic presentation with asymmetric rigidity, dystonia, and ideomotor
apraxia

• Marked asymmetry of involvement is the most striking feature and helps

differentiate CBD

• The most common presenting feature is asymmetric hand clumsiness

• Others-Early bradykinesia, a frontal syndrome, tremor, and rigidity

• Mean age of onset- sixth decade

• Mean survival- 7 years from diagnosis

Neuroimaging
• Asymmetric frontoparietal atrophy

• Fludeoxyglucose positron emission tomography (FDG-PET) - asymmetric

cortical metabolism

• Uptake on levodopa-positron emission tomography (DOPAPET)-Reduced

levodopa uptake in the striatum and highly asymmetric in the cortex

• CIT (iodine-123-2"-carbomethoxy-3"-[4-iodophenyl] tropane) SPECT shows a

similar pattern of reduced asymmetric striatal binding, but is nonspecific to CBD
(similar to dopamine transporter SPECT [DAT-SPECT])

chandra
Clinical Features
• Five initial presentations
• The most common presentation
• (55%) -"useless arm" (ie, a rigid, dystonic, akinetic, or apraxic arm),
• gait disorder (27%)
• prominent sensory symptoms
• isolated speech disturbance
• behavioural disturbance
Reward system and Executive function
• Brain reward system is a brain circuit that causes feelings of pleasure when it's
"turned on" .reinforces and alters behaviour.

• Neurons in the different regions of the brain comprising the reward system
communicate using dopamine:

• dopamine-producing neurons in the brain's ventral tegmental area

communicate with those in a region called the nucleus accumbens in order to
process rewards and to motivate behavior

Positive cortical tropism and the phenomena of agency

• The intend to capture system, intend to escape system and self awareness
system by efferent copy signal

• Frontal alien hand

• Classical alien hand
• Intermanual conflict
• Agnostic apraxia. When command is given for a hand the other hand does it.

• Diagonistic apraxia. Left hand does directionally opposite what the right does.

• Intermanual conflict. both hands complete the task but left undoes that
stealthily after done.

• Left hand constantly fights and inhibits the right

Slowness
• Loss of nigrostriatal dopamine causes akinesia /bradykinesia.

• Dopamine stimulates direct and inhibhit indirect pathway.

• All intrinsic basal ganglia pathways are dopaminergic except GABAergic in STN.
• When dopamine is depleted there is enhancement of GABA.

• This causes increased inhibhition of thalamocortical pathways and causes

bradykinesia or akinesia.

Function correlations with clinical features

• Freezing - transient inability to create effective stepping

• Festination - unintentional increase in speed, usually with small steps

• Periodic blinking is centrally located in brainstem reticular formation& basal

ganglia.

COEPS-2
• from supplementary motor area 6

• Centrally originating extrapyramidal system enters to putamen tegmentum and

nucleus of facial nerve.

• Nucleus accumbens to substantia nigra pars compacta connections are

important in the emotional behaviour of patients.

Swallowing & Bladder & constipation

• Higher control of swallowing

• Sense of food carried by 5,9,10 cranial

• Medulla co ordinates swallowing and respiration through meduallary network

involving tractus solitarius and respiratory centre.
• Insula & inferior frontal regions analyse relevance

• Central pattern to select or reject done by Basal ganglia, Reticular formation,

Cerebellum.

• Efferents direct bolus to oropharynx -vocal cord closes, larynx elevates

,pharyngeal constrictors constrict.

Bladder
• Associated autonomic involvement

• Onuf nucles pathology

• Barringtons centre or PMC (pontine micturitioncentre) relaxes the urethral

sphincter but goverened by higher [Link] in this mechanisms also
cause bladder symptoms
Sleep
• Altered sleep architecture -loss of atony in REM causing dream acting out.

• synucleinopathies, such as Parkinson's disease (PD), dementia with Lewy

bodies (DLB), and multiple system atrophy (MSA)

• Idiopathic or symptomatic

REM Sleep Behavior Disorder

• SPECT- reduced striatal dopamine transporters, & decreased striatal
dopaminergic innervation

• Treatment: Clonazepam highly effective, to 0.5 to 1.0 mg 90%, no tolerance or

abuse.

• Melatonin, Pramipexole or levodopa

• Therapeutic intervention-environmental safety.

How can we help?

• Individualize therapy:

• What is bothering you?

• Can I help this?

• Avoid treating non-bothersome symptoms

• Help by adding or subtracting medicines?

Dopamine Agonists

• Act on Dopamine receptors

• Effective in early disease

• Effective in managing motor complications

• Young onset PD

• Expensive

• Bromocriptine, Ropinirole and Piribedil available in India

• Pergolide, Pramipexole, Cabergoline available in India