The document discusses the extrapyramidal system and disorders of the extrapyramidal system. It begins by defining the extrapyramidal system as referring to the basal ganglia and array of brainstem nuclei. It then lists the components and tracts of the extrapyramidal system. The document goes on to discuss disorders like Parkinson's disease, classifying extrapyramidal disorders and listing clinical features. It also covers etiology, pathogenesis, diagnosis and treatment of Parkinson's disease.
This ppt describes various movement disorders found commonly in elderly persons. It also describes hyper and hypokinetic disorder categorization with cause and pathophysiology of movement disorders.
here i am to explain the Anatomy and physiology of part of the Pyramidal tract, that is the corticospinal tract. I also added the clinical significance of corticospinal tract. The course of the corticospinal tract are well explained.
MYOPATHIES A SPECIAL AND SEPERATE ENTITY WITH SPECIFIC FEATURES IN EACH DISORDER MAKING US EASY FOR DIAGNOSIS,CONFIRMATION BY MUSCLE BIOPSY.THE SEMINAR WAS PRSENTED ON 06/07/2011...AT 09.00AM
HAVE A LOOK ..AND COMMENT..WITHOUT BIAS..
Pyramidal tract by Sunita.M.Tiwale,Prof. Dept of physiology,D.Y.Patil Medical...Physiology Dept
Specific Learning Objectives:
At the end of session the students should be able to :
Enumerate the descending tracts.
Describe the origin, course, termination, collaterals of Pyramidal tract.
Describe the functions of the pyramidal tract.
Brown sequard syndrome or transverse hemisection syndrome
Causes symptoms and treatment of brown sequard syndrome
Background about the disease
Neural tracts
Ascending and descending pathways of the spinal cord (motor and sensory pathways)
Pathophysiology of brown sequard syndrome
This ppt describes various movement disorders found commonly in elderly persons. It also describes hyper and hypokinetic disorder categorization with cause and pathophysiology of movement disorders.
here i am to explain the Anatomy and physiology of part of the Pyramidal tract, that is the corticospinal tract. I also added the clinical significance of corticospinal tract. The course of the corticospinal tract are well explained.
MYOPATHIES A SPECIAL AND SEPERATE ENTITY WITH SPECIFIC FEATURES IN EACH DISORDER MAKING US EASY FOR DIAGNOSIS,CONFIRMATION BY MUSCLE BIOPSY.THE SEMINAR WAS PRSENTED ON 06/07/2011...AT 09.00AM
HAVE A LOOK ..AND COMMENT..WITHOUT BIAS..
Pyramidal tract by Sunita.M.Tiwale,Prof. Dept of physiology,D.Y.Patil Medical...Physiology Dept
Specific Learning Objectives:
At the end of session the students should be able to :
Enumerate the descending tracts.
Describe the origin, course, termination, collaterals of Pyramidal tract.
Describe the functions of the pyramidal tract.
Brown sequard syndrome or transverse hemisection syndrome
Causes symptoms and treatment of brown sequard syndrome
Background about the disease
Neural tracts
Ascending and descending pathways of the spinal cord (motor and sensory pathways)
Pathophysiology of brown sequard syndrome
Parkinson’s disease (PD):It is a progressive disorder of the central nervous system (CNS) with both motor and non-motor symptoms.
PD is a common disease that affects an estimated 1million American and an estimated 7 to 10 million people worldwide.
The prevalence of the disease is expected to increase substantially in the coming years due to the aging of the population.
The average age of onset is 50-60 years.
PATHOPHYSIOLOGY:
Parkinsonism is a generic term used to describe a group of disorders with primary disturbance in the dopamine system of basal ganglia (BG).
BG is a network of sub cortical nuclei consisting of caudate nucleus, putamen ,globus pallidus, and subthalamic nucleus with along with substantia nigra.
The BG engage in number of parallel circuit or loops ,only few of which are motor .
During my 1st &2nd year of residency period , i used to teach Anatomy and Orthopaedics for foreign undergraduate medical students. At last year i taught Neurology for one batch. so i posted some of my collections for competely educational purpose coz i believe in knowledge ...inseted of deleting these ppts , they may me useful for others so i shared it ....
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
2. The term extrapyramidal system, coined by British
neurologist Kinnier Wilson, refers to the BASAL
GANGLIA AND AN ARRAY OF BRAIN STEM
NUCLEI (red nucleus, reticular formation etc.) to which
they are connected.
Components of the extrapyramidal system include
Basal Ganglia,
The red nuclei
Vestibular nuclei,
Superior colliculus and
Reticular formation in the brain stem,
3. Basal ganglia and
Subcortical nuclei –
NAMES USED ARE AS
FOLLOWS
Caudate,putamen &
globus pallidus : corpus
straitum
Caudate & putamen
:straitum
Globus pallidus &
putamen : lentiform
nuclei
Globus pallidus :
pallidum
4. Extrapyramidal Tracts
They are consisted of a series of tracts:
•Rubrospinal Tract.
•Reticulospinal Tract,
Dividid into 2 types:
1. Pontine reticulospinal tract. (Medial)
2. Medullary reticulospinal tract. (Lateral)
•Tectospinal Tract.
•Vestibulospinal Tract.
5. Rubrospinal Tract
Originated from the red nucleus located in
the mesencephalon
Terminate in the lateral column
of spinal cord.
Function:Motor functions of skeletalmuscles
of the limbs, hands, and feet.
6. Reticulospinal Tract
A- pontine reticulospinal tract. (Medial & Excitatory)
Originated from pontine reticular nuclei in pons which terminate
in the medial anterior column.
anterior
B- Medullary reticulospinal tract. (Lateral & Inhibatory)
Originated from medulla and terminate in lateral
column.
Function: It Facilitates extensor reflexes & Inhibits Flexor
reflexes.
7. Tectospinal Tract
Origin: Superior colliculus of midbrain.
Terminate in the Anterior Column.
Function: Motor function of the Skeletal
muscles of the head and eyes in response to
visual stimuli.
8. Vestibulospinal Tract
Origin: vestibular nucleus in medulla.
Terminate in the Anterior Motor Neuron.
Function: Motor function of muscle for
maintaining balance in response to head
movements
9.
10.
11.
12. Phylogenetically, corpus striatum is primarily
responsible for stereotyped motor activities to
maintain tone, posture, locomotion and automatic
associated movement.
Regulation of voluntary motor activity
Control of the muscle tone
Maintenance of emotional and associative
movements
13. Disturbance in the control of voluntary motor activity resulting
in involuntary movements which may be of two main types:
Rhythmic and regular as in parkinsonism
Dysrhythmic and irregular as in chorea, athetosis and dystonia
Hypokinetic movements or Hyperkinetic movements are found
14. Extrapyramidal disorders are classified
broadly on clinical grounds into:
1. The akinetic-rigid syndromes in which
poverty of movements predominates
2. The dyskinesisas in which there are a
variety of excessive involuntary
movements
17. pyramidal system extrapyramidal system
function Skilful volitional
movements
Modulate volitional motor
movements
Finalizes an act Initiate an act
connection Direct linkage to
spinal cord
Multi neuronal and multi
synaptic via descending tracts
Cortico bulbar and
cortical spinal tract
reticulo-spinal, rubro-spinal,
olivo-spinal and vestibulo-spinal
tract.
Clinical features spasticity Rigidity( lead pipe/ cog wheel)
Reflexes brisk normal
Power diminished Usually not affected
Planters extensor flexor
Involuntary movements absent present
18. Age- age of disease onset is very important tourette
syndrome, typically begins in the first decade,
parkinsons disease usually occurs in late age
Past history –About infection (rheumatic fever),
jaundice(wilsons disease)
• Medical history & Toxin exposure
Drug history- of current, previous & recreational use
should be taken details : parkinsonism & dystonia
may be produced by dopamine receptor blocking
agent
Family history – should be taken and make a
pedigree chart if necessary (huntington disease)
19. Associated neuropsychiatric features –
Wilson disease, Huntington disease
Autonomic symptoms- dizziness,
bladder complaints, impotence etc may be
prominent & early in MSA,
neurodegenerative disease
, Alcohol responsiveness - essential
tremor is characteristically response to
alcohol
20. Specific distribution-
• Chorea/ athetosis - mainly in the distal groups
• Hemiballismus- mainly proximally
• Parkinsons disease- mainly unilateral & asymmetric
• Blepherospasm- affect both eye
Specific action & relationship to voluntary
movement-
• task specific tremor (intention tremor) during pick up a
glass of water
• Task specific dystonia eg: Writers cramp, musician
cramp
21. Speed of movement-
Rhythm-
Continuous – tremor
Intermittent – astrexis
Relationship to sleep- Palatal myoclonus,
segmental myoclonus, fasciculation &
myokymia, persist during sleep , Dystonia
diminished on sleep
Supresibility- tics may be voluntary suppressed
Slow Intermediate Fast
Parkinsonism Chorea Myoclonus
Dystonia Tremor Tics
Athetosis
22. Aggravating or precipitating factor- stress and anxiety
worsen all movement disorder
• Myoclonus may be triggered by specific stimuli-
sudden loud noise or touch
• Carbohydrate heavy meal, fatigue may precipitate
paroxysmal dystonia
Associated sensory symptom- RLS
associated with pain or discomfort, tics may be
associated with vague discomfort or abnormal
sensation
Ameliorating factor- alcohol dramatically
improved essential tremor and myoclonic
dystonia
23. • Parkinson's disease (PD) is the second
commonest neurodegenerative disease.
• It is estimated 1 million persons in the US
• 5 million persons in the world.
• English doctor James Parkinson, who
published the first detailed description in An
Essay on the Shaking Palsy in 1817
PARKINSON’S DISEASE
24. Clinical Features of Parkinson's Disease
Cardinal Features
Bradykinesia
Rest tremor
Rigidity
Other Motor Features
Micrographia Masked
facies
(hypomimia)equalize
Gait disturbance/postural Reduced eyeblink
Dysphagia
Freezing
Nonmotor Features
Anosmia
Sensory disturbances
(e.g., pain)
Mood disorders (e.g.,
instability Soft voice (hypophonia) depression)
Sleep disturbances
Autonomic disturbances
Orthostatic hypotension
Gastrointestinal
disturbances
Genitourinal disturbances
Sexual dysfunction
Cognitive
impairment/Dementia
25. • AGE -The most important risk factor
• Positive family history
• Male gender
• Environmental exposure: Herbicide and pesticide
exposure, metals (manganese, iron), well water, farming,
rural residence, wood pulp mills; and steel alloy industries
• Life experiences (trauma, emotional stress, personality
traits such as shyness and depressiveness)
Risk factors of PD
27. 1- Static tremors
Rhythmic occuring at a rate of 4-8 / second
May start in one hand and spread to other
parts of the body
Characteristically pill-rolling movements
between the thumb and the forefinger are
seen
Tremors increase with emotional, anxiety and
fatigue and disappear during sleep and during
active voluntary movements
28. 2- Rigidity of the muscles
More proximal than distal
Flexors are affected more than extensor
On clinical examination the resistance may be
continuous throughout the act to the same
degree (lead pipe rigidity) or interrupted by
the tremors (cog wheel rigidity)
Stiffness of the limbs develops causing
difficulty in starting movements and walking
(slow, shuffling gait)
29. 3- Akinesia: Loss of emotional and
associative movements resulting in:
Immobile face with infrequent blinking
(mask face)
Monotonous speech
Loss of swinging of the arms during
walking
30. Pathologically, the HALLMARK FEATURES OF PD ARE
DEGENERATION OF DOPAMINERGIC NEURONS IN THE
SUBSTANTIA NIGRA PARS COMPACTA (SNC), reduced
striatal dopamine, and intracytoplasmic proteinaceous
inclusions known as Lewy bodies.
Neuronal degeneration with inclusion body formation can also
affect
cholinergic neurons of the nucleus basalis of Meynert (NBM),
norepinephrine neurons of the locus coeruleus (LC),
serotonin neurons in the raphe nuclei of the brainstem,
and neurons of the olfactory system, cerebral hemispheres,
spinal cord, and peripheral autonomic nervous system.
31. It has been proposed that most cases of PD are due to a
"DOUBLE HIT" involving an interaction between a gene
mutation that induces susceptibility coupled with exposure to
a toxic environmental factor.
The most significant of these mechanisms appear to be
protein misfolding and accumulation and mitochondrial
dysfunction.
Lewy bodies and Lewy neurites, which are composed of
misfolded and aggregated proteins.
PD – Etiology and Pathogenesis
37. Three cardinal symptoms:
1. Resting tremor
2. Bradykinesia (generalized slowness of
movements)
3. Muscle rigidity
Symptoms worsen as disease progresses.
Clinical features of PD
38. Resting tremor: Most common first
symptom, most evident in one hand
with the arm at rest.
♦ usually unilateral
♦ becomes bilateral
♦ worsens with stress
39. Tremors
Usually –
♦ first symptom
♦ occurs in the hands or arms can occur in head,
face, jaw, & leg
♦ disappears with purposeful movement
41. Patients also suffer from non- motor symptoms such as:
♦ cognitive impairments
♦ olfactory impairments
♦ dysphagia
♦ GI dysfunction
♦ sleep disturbances
♦ depression
42. Modern immunocytochemical techniques and genetic findings
suggest that Parkinson-plus syndromes can be broadly grouped
into 2 types: SYNUCLEINOPATHIES AND TAUOPATHIES.
Clinically, however, 5 separate Parkinson-plus syndromes have
been identified, as follows:
1. Multiple system atrophy
2. Progressive supranuclear palsy
3. Parkinsonism-dementia-amyotrophic lateral sclerosis complex
4. Corticobasal ganglionic degeneration
5. Diffuse Lewy body disease
Parkinson-plus syndromes respond poorly to the standard
treatments for Parkinson disease (PD).
43.
44. DIAGNOSIS
Parkinsonism is predominantly DIAGNOSED
CLINICALLY.
However, the other investigations helpful are :
1. MRI
2. SPECT Imagining
3. Biopsy useful in case of Parkinsonism Plus
Syndromes
4. Autopsy specimen to confirm the diagnosis
47. Drugs commonly used in
the treatment of
Parkinson disease
MEDICATION
Carbidopa-L-dopa
(Sinemet)
MAIN BENEFIT
Reduction of tremor and
bradykinesia; less effecton
postural difficulties
SIDE EFFECTS
Nausea, dyskinesias, orthostatic
hypotension, hallucinations,
confusion, arrhythmia
Controlled release
carbidopa-L-dopa
Dopamine agonists
Ropinirole(D3)
Moderate effects on all
aspects; reduced motor
fluctuations of L-dopa,
neuroprotective, neurotrophic
Orthostatic hypotension,
excessive and abrupt
sleepiness, confusion,
hallucinations, impulse control
disorders
Pramipexole(D2)
48. Tremor reduction, less effect
on other features, drug
Atropinic effects: dry mouth,
urinary outlet obstruction,
confusion and psychosisInduced parkinsonism
Neuroprotection, adjuntive
therapy
Insomnia
Anticholinergics
Benztropine
(Cogentin)
Trihexyphenidyl
(Artane)
MAO-B inhibitor
selegiline,
Rasagiline
COMT inhibitors
Entacapone
Urine discoloration, diarrhea,
increased dyskinesias
Glutamate agonist
Amantadine
(Symmetrel)
Smoothing of motor
fluctuations
Leg swelling, congestive heart
failure, prostatic outlet
obstruction, confusion,
hallucinations, insomnia
49. Contrary to dopamine, it can pass into the brain
where it is decarboxylated into dopamine
Levodopa is combined with a peripheral L-AA
decarboxylase inhibitor e.g. carbidopa or
benserazid to
delivery of l-dopa into the brain
peripheral adverse effects of dopamine
Carbidopa if peripheral adverse effects are
prominent
It has dramatic initial response, decreases with
time (wear off) due to the progressive loss of
neurons
50.
51. Combined with carbidopa is the most
potent oral therapy for Parkinson’s disease
Symptoms of Parkinson’s disease but
does not stop the progression
(deterioration) of the disease i.e.
Symptomatic treatment
From the third year its efficacy declines
54. Have longer duration less fluctuation
Have less tendency to induce dyskinesia
Ineffective in patients not responding to
levodopa
Can be used in early cases to delay use
of levodopa (in levodopa-naïve patients) & in
advanced cases to augment
levodopa and to decrease fluctuations to
its response
55. Pergolide is more potent than Bromocriptine
Their side effects limit their use and slow rapid
build up of doses (over 2-3 Months)
Side effects include levodopa side effects in
addition to spasmogenicity & fibrosis (of serous
membranes)
ERGOT DERIVATIVES
56. Pramipexole & Ropinirole
Pramipexole: is cleared by renal
excretion
Ropinirole: is cleared by liver metabolism
Side effects as levodopa with less
dyskinesia and fluctuation and
No spasmogenicity and fibrosis
57. Antiviral (influenza) drug
The mode of action is unknown
• NMDA glutamate receptors (the primary action)
• Muscarinic receptors
• Increases release of dopamine
It has little effect on tremors &
Tolerance develops rapidly
58. Augment the effect of dopamine
Weak and play an adjuvant role
They are the same in efficacy but with some inter-
individual variation in response
Side effects:
Mood changes
Xerostomia, blurred vision, constipation, urinary
retention
Hallucination, confusion
C/I: in glaucoma, SPH, Pyloric stenosis
59. PARKINSON PLUS SYNDROME
THE RESPONSETO DRUGS ARE POOR WHENTHE PATIENT HAS PARKINSONS PLUS
SYNDROME.
Clinical clues suggestive of Parkinson-plus syndromes include the
following:
Early onset of dementia
Early onset of postural instability
Early onset of hallucinations or psychosis with low doses of
levodopa/carbidopa or dopamine agonists
Ocular signs, such as impaired vertical gaze, blinking on saccade,
square-wave jerks, nystagmus, blepharospasm, and apraxia of eyelid
opening or closure
Pyramidal tract signs not explained by previous stroke or spinal cord
lesions
Autonomic symptoms such as postural hypotension and incontinence
early in the course of the disease
Prominent motor apraxia
Alien-limb phenomenon
Marked symmetry of signs in early stages of the disease
Truncal symptoms more prominent than appendicular symptoms
Absence of structural etiology such as a normal-pressure hydrocephalus
(NPH)
60.
61. Stereotactic neurosurgery: pallidotomy, thalamotomy ,sub
thalamotomy
Indications
1.idiopathic parkinsons
2.levodopa unhelpful
3.intractable PD
4.drug dyskinesias
Deep brain stimulation: dyskinesia
Tissue transplantation: Experimental transplantation of fetal
or autologous dopamine-containing adrenal medulla or stem
cell research has produced no promising results in PD to date.
Physiotherapy and physical aids
Neuropsychiatric aspects: Cognitive impairment and
depression are common as PD progresses. SSRIs are the
drugs of choice for depression.
62. • Associated with drugs, stroke, tumour, infection, or
exposure to toxins such as carbon monoxide or
manganese.
SECONDARY PARKINSONISM
63. •Side effects of some drugs, especially those that affect
dopamine levels in the brain, can actually cause symptoms of
Parkinsonism.
•Although tremor and postural instability may be less severe,
this condition may be difficult to distinguish from Parkinson’s
disease.
• Medications that can cause the development of Parkinsonism
include:
– Antipsychotics
– Metaclopramide
– Reserpine
– Tetrabenazine
– Some calcium channel blockers
– Stimulants such as amphetamines and cocaine
– Usually after stopping those medications Parkinsonismgradually
disappears
Drug-induced Parkinsonism
64. • Multiple small strokes can cause Parkinsonism.
• Patients with this disorder are more likely to present
with gait difficulty than tremor, and are more likely to
have symptoms that are worse in the lower part of the
body.
• Some will also report the abrupt onset of symptoms or
give a history of step-wise deterioration (symptoms get
worse, then plateau for a period).
• Dopamine is tried to improve patients’mobility
although the results are often not as successful.
• Vascular Parkinsonism is static (or very slowly
progressive) when compared to other
Vascular Parkinsonism
65. •Atypical parkinsonism refers to a group of neurodegenerative
conditions that usually are associated with MORE WIDESPREAD
NEURODEGENERATION THAN IS FOUND IN PD (often
involvement of SNc and striatum and/or pallidum).
•As a group, they PRESENT WITH(RIGIDITY AND
BRADYKINESIA) but typically have a slightly different clinical
picture than PD, reflecting differences in underlying pathology.
•In the EARLY STAGES, THEY MAY SHOW SOME
MODEST BENEFIT FROM LEVODOPA and be difficult
to distinguish from PD.
PARKINSON PLUS SYNDROME
66. •NEUROIMAGING of the dopamine system
is USUALLY NOT HELPFUL, as several
•Atypical parkinsonisms also have degeneration
of dopamine neurons. Pathologically,
neurodegeneration occurs without Lewy bodies
67. Metabolic imaging of the basal ganglia/thalamus network may be
helpful, reflecting a pattern of decreased activity in the GPi with
increased activity in the thalamus, the reverse of what is seen in
PD.
TYPES ATYPICAL PD.
•Progressive Supranuclear Palsy (PSP)
•Corticobasal Degeneration (CBD)
•Multiple System Atrophy (MSA)
Shy-Drager syndrome (DSD), Striatonigral degeneration (SND) and
OlivoPontoCerebellar Atrophy (OPCA).
PARKINSON PLUS SYNDROME