More than 10 million people suffer from epilepsy in India.Seizures impact the lives of people with epilepsy and their family in many ways including creating barriers to employment and education and facing a sense of discrimination and isolation from their peers who donʼt understand what happens when they see a seizure occur. In India, epilepsy is still thought of as mental illness mainly due to lack of information on the condition among the general public.
This presentation touches every aspect of epilepsy
1. Overview of Epilepsy;
2. Type of Seizures;
3. Diagnosis and Management;
4. Psychological Issues; and
5. Social Perspectives.
A brief presentation about confusional states. Difference between coma. This presentation is focused on Pathophysiology, major causes and approach to diagnosis and diagnosis tools.
More than 10 million people suffer from epilepsy in India.Seizures impact the lives of people with epilepsy and their family in many ways including creating barriers to employment and education and facing a sense of discrimination and isolation from their peers who donʼt understand what happens when they see a seizure occur. In India, epilepsy is still thought of as mental illness mainly due to lack of information on the condition among the general public.
This presentation touches every aspect of epilepsy
1. Overview of Epilepsy;
2. Type of Seizures;
3. Diagnosis and Management;
4. Psychological Issues; and
5. Social Perspectives.
A brief presentation about confusional states. Difference between coma. This presentation is focused on Pathophysiology, major causes and approach to diagnosis and diagnosis tools.
Learn about coma/lethergy/stupor/lockdown syndrome
Unconscious.
In psychiatry, it is always difficult to distinguish the different reduce level of conscious states from catatonia.
This presentation shows more light about coma and how we differentiate it from other forms
Learn about coma/lethergy/stupor/lockdown syndrome
Unconscious.
In psychiatry, it is always difficult to distinguish the different reduce level of conscious states from catatonia.
This presentation shows more light about coma and how we differentiate it from other forms
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
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
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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
2. • Determine the disease causing diminished state of
unconsciousness
• Determine the direction in which it is evolving
To protect the brain against irreversible damage
3. Most common causes of diminished consciousness
1. Metabolic and diffuse disorders (65%)
• Drug poisoning
• Ischemia or anoxia
• Hepatic encephalopathy
• Encephalomyelitis and encephalitis
• Subarachnoid hemorrhage
• Endocrine disorders (including diabetes)
• Acid-base disorders
• Uremic encephalopathy
4. Most common causes of diminished consciousness
2. Supratentorial mass lesions (20%)
• Intracerebral hematoma
• Subdural hematoma
• Cerebral infarct
• Brain tumor
• Brain abscess
• Epidural hematoma
• Thalamic infarct
• Pituitary apoplexy
5. Most common causes of diminished consciousness
3. Subtentorial lesions (13%)
• Brainstem infarct
• Pontine hemorrhage
• Cerebellar hemorrhage
• Cerebellar tumor
• Cerebellar infarct
4. Psychiatric disorders (3%)
6. Consciousness
State of awareness of self and environment
AND
normal responsiveness to external stimulation and inner need.
Normal consciousness may fluctuate during the day
BUT
the normal individual can be brought immediately to a state of full
alertness and function.
7. Confusion
Inability to think with customary speed, clarity, and coherence.
Some degree of inattentiveness and disorientation i.e. Distractibility
and imperceptiveness.
“Clouding of sensorium”
Results most often from process that influences the brain globally, such
as a toxic or metabolic disturbance or dementia or sleep deprivation.
8. Salient features of a confused individual:
• Severely confused and inattentive persons are unable to do more
than carry out the simplest commands.
• Speech may be limited to a few words or phrases but some confused
individuals are voluble (~Talkative).
• Disoriented in time and place
• Do not grasp their immediate situation
• Do not understand the predicament of their own confusion
• May misidentify people or objects.
• These illusions may lead to fear or agitation.
• Loss of capacity to recall events of the past hours or days
• Deficit in working memory
9. Delirium = Confusion (Adams and Victor)
Delirium: Acute confusional state (Harrison’s)
10. Drowsiness
Inability to sustain a wakeful state without application of external
stimuli.
Sustain alertness for at least some brief period, without the further
necessity of external stimuli
Some degree of inattentiveness and mild confusion are present,
improving with arousal.
The patient shifts positions somewhat naturally and without
prompting.
The lids droop; there may be snoring, the jaw and limb muscles are
slack, and the limbs are relaxed.
11. Stupor
A state in which the patient can be roused only by vigorous and repeated
stimuli
Arousal cannot be sustained without repeated stimulation.
Responses to spoken commands are either absent or slow and inadequate.
Restless or stereotyped motor activity is common.
Reduction or elimination of the natural shifting of body positions.
When left unstimulated, these patients quickly drift back into a deep sleep-
like state.
The eyes are usually found to be displaced outward and upward, a feature
that is shared with sleep.
12. Vegetative state
• Person is awake but is showing no signs of awareness.
• Preserved autonomic and respiratory function without cognition
• Open their eyes
• Wake up and fall asleep at regular intervals
• Have basic reflexes (such as blinking when they're startled by a loud
noise or withdrawing their hand when it's squeezed hard)
• Able to regulate their heartbeat and breathing without assistance.
BUT
the patient regains neither awareness nor purposeful behavior.
13. Persistent Vegetative State
• Vegetative state for 3 months after non traumatic brain injury
• Vegetative state for 12 months after traumatic brain injury
• Also known as Apallic syndrome or Neocortical death
Multi-Society Task Force on PVS concluded that the outcome from a
vegetative state is better in traumatic as compared to nontraumatic
cases.
14. Vegetative state vs Coma
• A coma is when a person shows no signs of being awake and no signs
of being aware
• A vegetative state is when a person is awake but is showing no signs
of awareness
15. Minimally conscious state
• Patient is capable of some rudimentary behavior
• Following a simple command, gesturing, or producing single words or
brief phrases
• Demonstrate a degree of awareness
• Inconsistent from one examination to other
• Transitional or permanent state
• Continuum of vegetative state. Less severe but profound dementia
16. Locked in syndrome (Deefferented state)
• Little or no disturbance of consciousness
• Inability to respond adequately with motor activity and speech
• Most often caused by a large lesion of the ventral pons (basis pontis),
usually as a result of occlusion of the basilar artery
• Spare both the somatosensory pathways, and the ascending neuronal
systems responsible for arousal and wakefulness
• Spare certain midbrain elements that allow the eyelids to be raised in
wakefulness
• Interrupts the descending corticobulbar and corticospinal tracts
• Can respond by voluntary vertical gaze and blinking
17. Akinetic mutism
• Inert (akinetic) and silent (mutism)
• Bilateral lesions in anterior part of frontal lobe or thalamus
• Motor and sensory pathways are intact
• Profoundly apathetic
• Marked delay in verbal and motor response (Abulia)
• Intense stimulation May speak normally and relate the events
18. Catatonia
• Unresponsive
• Can simulate stupor, light coma or akinetic mutism
• No signs of structural brain damage (Normal pupillary reaction,
normal reflexes)
• Oculocephalic reflex is muted.
• Resistance to eye opening
• Waxy flexibility to passive limb movement
• Long periods of uncomfortable limb positions (Catalepsy)
• EEG shows normal alpha activity that is attenuated by stimulation
19.
20. Electroencephalogram (EEG) in states of
impaired consciousness
Confusion/Drowsiness
• Disappearance of normal alpha rhythm
• Replacement by random slow waves of low to moderate voltage
Stupor
• Regular slow waves (2-3 Hz) of high voltage
Deep coma
• Slow, low voltage waves
• Intermittent suppression of electrical activity
Brain death
• Complete absence of electrical activity
21. EEG in impaired consciousness due to
metabolic disorders
Hepatic or renal failure (Uremia)
• Slow waves
• High voltage
Coma due to sedatives intoxication
• Beta activity replaces normal rhythm
Delta pattern
Triphasic waves
22. Deeply comatose patients
• Diffuse transient alpha activity
• Also known as alpha coma
• Can be mistaken for normal activity
BUT
• No reactivity to sensory stimuli
Associated with pontine or diffuse cortical lesions
Poor prognosis
24. Anatomy and neurophysiology of alertness
and coma
Reticular Activating System (RAS)
• Indistinct boundaries
• Neurons are interspersed
• Locus coeruleus: Upper dorsolateral pons of the brainstem. Activated
directly by orexin from the lateral hypothalamus. Nor-epinephrine
• Raphe nuclei: midline throughout the brainstem within the pons, midbrain,
and medulla. Serotonergic
• Tuberomamillary nucleus: located within the posterior aspect of the
hypothalamus. Histaminergic
• Lateral and dorsal pedunculopontine tegmentum: Primarily cholinergic
neurons in neighboring groups within the midbrain and pons. Cholinergic
neurons project to the thalamus and cortex.
26. RAS receives collaterals from the spinothalamic and trigeminal–
thalamic pathways
Project to the whole of the cerebral cortex, not just to the sensory
cortex of parietal lobe
Cerebral cortex also modulates afferent sensory stimulus towards the
RAS through corticofugal projections
27. Pathologic basis of vegetative state
• Diffuse cerebral injury as a result of closed head trauma
• Widespread necrosis of the cortex after cardiac arrest or other form
of anoxia
• Thalamic necrosis
Prominent pathologic changes are often in the thalamic and
subthalamic nuclei rather than solely in the cortex.
28. In traumatic cases, the pathologic findings are often of diffuse
subcortical white matter degeneration (described as diffuse axonal
injury), prominent thalamic degeneration, and ischemic damage in the
cortex.
Anatomic findings indicate that PVS is a state in which the cortex is
either diffusely injured or effectively disconnected and isolated from
the thalamus, or the thalamic nuclei are destroyed
29. Pathologic anatomy of coma
Two broad processes
1. Structural, or morphologic, consisting either of a discrete structural
lesion in the upper brainstem and lower diencephalon (which may
be primary or secondary to compression) or of more widespread
destructive changes throughout the hemispheres.
2. Metabolic or submicroscopic, resulting in suppression of neuronal
activity in the cerebrum and reticular activating system.
30. Structural or morphological
1. A large mass in one cerebral hemisphere— tumor; abscess; massive
infarct; or intracerebral, subdural, or epidural hemorrhage.
Cause coma by secondary compression of the midbrain and central
thalamic region of the RAS.
Displacement or direct compression of these structures by the
advancing medical temporal lobe which is forced into the tentorial
opening.
OR
cerebellar lesion may compress the adjacent upper brainstem reticular
region by displacing it forward and upward
31. Structural or morphological
2. Destructive lesion is located immediately within the thalamus or midbrain,
in which case the neurons of the RAS are damaged directly.
Brainstem stroke from basilar artery occlusion, thalamic and upper brainstem
hemorrhages, and some forms of traumatic damage.
3. Widespread bilateral damage to the cortex and cerebral white matter, the
result of traumatic damage (contusions, diffuse axonal injury), bilateral
ischemic strokes or hemorrhages, encephalitis, meningitis, hypoxia, or global
ischemia.
The coma in these cases results from interruption of thalamocortical impulses
or from generalized destruction of cortical neurons. It is only if the cerebral
lesions are bilateral and extensive that consciousness is impaired. Many of
the diseases in this category also cause severe thalamic damage.
32. Coma in concussion
• Transient but large increase in intracranial pressure
• 200 to 700 lb/in2 (10000-36000 mmHg)
• Lasting a few thousandths of a second
• Vibration set up in the skull and transmitted to the brain was for many
years thought to be the basis of the abrupt paralysis of nervous function
that characterizes concussive head injury (commotio cerebri).
• Sudden swirling motion of the brain induced by acceleration or
deceleration from a blow to the head produces a rotation (torque) of the
cerebral hemispheres around the axis of the upper brainstem.
If severe: multiple shearing lesions or hemorrhages in diencephalon and
brain stem.
33. ‘In the largest group of cases of coma, no structural lesion is
revealed by any technique of conventional pathology.’
34. Metabolic and toxic encephalopathies
• Cerebral Blood Flow (CBF): 55mL/min/100g
• Reduction in cerebral blood flow
• Cerebral blood flow may stay near normal while metabolism is greatly
reduced
35. Clinical approach to comatose patient
• Often, comatose patient is brought to the hospital and little pertinent
medical information is available.
• BLS/ACLS
• If history or suspicion of trauma: ATLS (ABCDE) approach.
36. • Patient’s airway is cleared and blood pressure is restored.
• Patient’s airway is cleared and blood pressure is restored.
• With hypotension, placement of a central venous line and administration
of fluids, pressor agents and blood.
• If respirations are shallow or labored, or if there is emesis with a threat of
aspiration, tracheal intubation and mechanical ventilation are instituted.
• An oropharyngeal airway is otherwise adequate in a comatose patient who
is breathing normally.
• Deeply comatose patients with shallow respirations require endotracheal
intubation.
• The patient with a head injury may also have suffered a fracture of the
cervical vertebrae, in which case caution must be exercised in moving the
head and neck.
37. • Circumstances in which the person was found.
• Previous health, whether there was a history of diabetes, a head
injury, convulsion, alcohol or drug use, or a prior episode of coma or
attempted suicide.
• Sedatives, antiepileptic drugs, opiates, certain antibiotics,
antidepressants, and antipsychotic drugs.
38. General examination : Vitals
Temperature
Fever
• Systemic infection (eg. Pneumonia, meningitis, viral encephalitis)
• Temperature >107.6F: Heat stroke, anticholinergic drug intoxication
• Central fever is rare
Hypothermia
Alcohol or barbiturate intoxication
Drowning
Cold exposure
Advanced TB meningitis
39. General examination : Vitals
Respiration
Slow breathing: opiate or barbiturate intoxication, hypothyroidism
Deep rapid (Kussmaul respiration) : pneumonia, diabetic or uremic
acidosis, pulmonary edema, or the less-common occurrence of an
intracranial disease that causes central neurogenic hyperventilation.
Slow, irregular, or cyclic (Cheyne-Stokes respiration) : Raised ICP
40. General examination : Vitals
Respiration
Apneustic breathing (Pause 2-3s after inspiration) : Low pontine lesion
Biot breathing/Ataxia of breathing (chaotic, being irregularly interrupted
and each breath varying in rate and depth) : Dorsal medulla lesion
41. Cheyne-Stokes respiration
• Isolation of the brainstem respiratory centers from the cerebrum,
rendering them more sensitive than usual to carbon dioxide
(hyperventilation drive)
• Signifies bilateral dysfunction of cerebral structures
• Intoxication or a metabolic derangement
• Bilateral structural lesions such as subdural hematomas
42. General examination : Vitals
Blood pressure
Hypertension: cerebral hemorrhage, hypertensive encephalopathy and in
children with markedly elevated intracranial pressure.
Hypotension: Alcohol or barbiturate intoxication, DKA, internal
hemorrhage, myocardial infarction, dissecting aortic aneurysm,
septicemia, Addison disease, or massive brain trauma.
43. General examination : Vitals
Heart rate
Bradycardia
• Heart block from medications such as tricyclic antidepressants or
anticonvulsants
• If combined with periodic breathing and hypertension, an increase in
intracranial pressure.
44. Neurological examination
Inspection
• Predominant postures of the limbs and body
• Presence or absence of spontaneous movements on one side
• Position of the head and eyes
• Rate, depth, and rhythm of respiration
46. Pupillary reaction
• Loss of light reaction usually precedes enlargement of pupil
• Unilaterally enlarged (“Hutchinson”) pupil : Early indicator of
stretching or compression of the third nerve. Presence of an overlying
ipsilateral hemispheral mass.
• The light-unreactive pupil continues to enlarge to a size of 6 to 9 mm
diameter and soon, there is slight outward deviation of the eye.
• As midbrain displacement continues, both pupils dilate and become
unreactive to light as a result of compression of the oculomotor
nuclei in the rostral midbrain.
47. Pupillary reaction
• Pontine tegmental lesions (eg. Pontine hemorrhage) : extremely
miotic pupils (<1 mm in diameter) with barely perceptible reaction to
strong light.
• Ipsilateral pupillary dilatation from pinching the side of the neck (the
ciliospinal reflex) is usually lost in brainstem lesions.
• The Horner syndrome (miosis, ptosis, and reduced facial sweating):
ipsilateral to a lesion of the brainstem or hypothalamus or as a sign of
dissection of the internal carotid artery.
48. Coma caused by drug intoxications and intrinsic metabolic disorder
• Pupillary reactions are usually spared
Exceptions
• Serum concentration of opiates that are high enough to cause coma
Pinpoint pupils
• Systemic poisoning with atropine or with drugs that have atropinic
qualities, especially the tricyclic antidepressants or SSRI: dilatation
and relative unresponsiveness to light
49.
50. Movements of eye, eyelids and corneal
reaction
• Stupor or light coma of metabolic origin:
Eyes rove conjugately from side to side in seemingly random fashion.
Disappears as coma deepens motionless and exotropic
• Lateral and slight downward deviation: third-nerve palsy on that side
• Medial deviation : Sixth-nerve palsy on that side
51. Movements of eye, eyelids and corneal
reaction
Conjugate deviation of the eyes away from the side of the paralysis: large
cerebral lesion (looking toward the lesion)
Toward the side of the paralysis: unilateral pontine lesion (looking away from
the lesion)
Retraction and convergence nystagmus: lesions in the tegmentum of the
mid-brain
Ocular bobbing: lesions of the tegmentum of the pons
Down and inward (looking at the nose): hematomas or ischemic lesions of
the thalamus and upper midbrain (a variant of Parinaud syndrome)
“Ocular dipping,” (eyes move down slowly and return rapidly to the
meridian) : Anoxia and drug intoxications
53. Elicitation of these ocular reflexes in a comatose patient:
1. evidence of unimpeded function of the midbrain and pontine
tegmental structures that integrate bi-ocular eye movements
2. intactness of the CN nerves (III, IV, and VI) on both sides
54. Caloric test / vestibulo-ocular test
More vigorous stimulus for ocular movements in coma is accomplished
by irrigation of one ear with 10 mL of cold water (or room-temperature
water if the patient is still arousable).
Causes slow conjugate deviation of the eyes toward the irrigated ear,
followed in a few seconds by compensatory nystagmus (fast
component away from the stimulated side).
In comatose patients, the fast “corrective” phase of nystagmus that is
mediated by the frontal lobes is lost and the eyes are tonically
deflected.
55. Reduction in the frequency and eventual loss of spontaneous blinking
Loss of response to touching the eyelashes Lack of response to
corneal touch (the corneal reflex afferent limb travels in the trigeminal
nerve and efferent limb travels in facial nerve) : signs of deepening
coma
56. Sequentially increasing stimuli
• calling his name
• simple commands
• noxious stimuli such as tickling the nares, supraorbital or sternal
pressure, pinching the side of the neck or inner parts of the arms or
thighs, or applying pressure to the knuckles
57. Vocalization may persist in stupor and will be the first response to be
lost as coma appears.
Grimacing and deft avoidance movements of stimulated parts
of the body are preserved in stupor.
Yawning and spontaneous shifting of body positions indicate a minimal
degree of unresponsiveness.
58. Hemiplegia
• Lack of restless movements of the limbs
• Inadequate protective movements in response to painful stimuli.
• The weakened limbs are usually slack and, if lifted from the bed, they
“fall flail.”
• The hemiplegic leg lies in a position of external rotation
• Affected thigh appears wider and flatter than the nonhemiplegic one.
In expiration, the cheek and lips puff out on the paralyzed side of the
face.
A lesion in one cerebral hemisphere causes the eyes to be turned away
from the paralyzed side (toward the lesion).
The opposite occurs with brainstem lesions.
In most cases, a hemiplegia and an accompanying Babinski sign are
indicative of a contralateral hemispheral lesion.
59. Posturing
Decerebrate rigidity
• Opisthotonos
• clenching of the jaws
• stiff extension of the limbs
• internal rotation of the arms and plantar flexion of the feet
Lesions that interrupt the fibers of the red nucleus lead to inhibition of
the rubrospinal tract (To flexor muscles) and constant excitation of the
vestibulospinal and pontine reticulospinal tracts (To extensor muscles)
60. Posturing
Decorticate rigidity
• Arms in flexion and adduction and legs extended.
• Lesions at a more rostral level of the nervous system—in the cerebral
white matter or internal capsule and thalamus.
If preceded by decorticate or decerebrate postures, the coma is
profound and usually progresses to brain death.
61. Clinical signs of raised ICP
• History of headache before the onset of coma
• Vomiting,
• Severe hypertension beyond the patient’s static level
• Unexplained bradycardia
• Retinal hemorrhages
62. • Papilledema
Develops within 12 to 24 h in cases of brain trauma and hemorrhage
If seen at presentation with coma, signifies brain tumor or abscess
(lesion of longer duration)
Absence of papilledema does not exclude the presence of increased
intracranial pressure, particularly in the elderly.
63. Acute Hydrocephalus
• Subarachnoid hemorrhage or from obstruction of the ventricular
system by a tumor in the posterior fossa
• Abulia Stupor Coma
• Pupils: small and the tone in the legs is usually increased or there may
be extensor posturing.
64. Classification of Coma
1.Diseases that cause no focal or lateralizing neurologic signs, usually
with normal brainstem functions. CT scan and cellular content of the
CSF are normal
A. Exogenous intoxications: alcohols, barbiturates and other sedative
drugs, opiates
B. Endogenous metabolic disturbances: anoxia, diabetic acidosis,
uremia, hepatic failure, nonketotic hyperosmolar hyperglycemia, hypo-
and hypernatremia, hypoglycemia, addisonian crisis, profound
nutritional deficiency, carbon monoxide poisoning, thyroid states,
hypercalcemia
C. Severe systemic infections: pneumonia, peritonitis, typhoid fever,
malaria, septicemia, Waterhouse- Friderichsen syndrome
65. Classification of Coma
D. Circulatory collapse (shock) from any cause
E. Postseizure states
F. Hypertensive encephalopathy and eclampsia
G. Hyperthermia and hypothermia
H. Concussion
I. Acute hydrocephalus
66. Classification of Coma
2. Diseases that cause meningeal irritation and an excess of white
blood cells (WBCs) or red blood cells (RBCs) in the CSF, usually without
focal or lateralizing cerebral or brainstem signs
A. Subarachnoid hemorrhage from ruptured aneurysm, arteriovenous
malformation, and cerebral trauma.
B. Acute bacterial meningitis
C. Viral meningoencephalitis
D. Neoplastic meningeal infiltration
E. Parasitic meningitis
F. Pituitary apoplexy
67. Classification of Coma
3. Diseases that cause focal brainstem or lateralizing cerebral signs, with or
without changes in the CSF.
A. Hemispheral hemorrhage or massive cerebral infarction
B. Brainstem infarction caused by basilar artery thrombosis or embolism
C. Brain abscess, subdural empyema, herpes encephalitis
D. Epidural and subdural hemorrhage and brain contusion
E. Brain tumor
F. Cerebellar and pontine hemorrhage
G. Multiple focal cerebral lesions that cumulate to cause generalized brain
dysfunction: multiple embolic infarction caused by bacterial endocarditis,
TTP, sagittal sinus thrombosis, diffuse fat embolism.