PROGRESSIVE SUPRANUCLEAR PALSY-MRI SPOTTER WITH OTHER IMAGING SIGNSKannan Narayanan S
Atypical parkinsonism is a group of neurodegenerative disorders where parkinsonism is a prominent feature but differs from IPD by associated atypical features.
References-Harrison textbook of Internal medicine,Various sourcres
PROGRESSIVE SUPRANUCLEAR PALSY-MRI SPOTTER WITH OTHER IMAGING SIGNSKannan Narayanan S
Atypical parkinsonism is a group of neurodegenerative disorders where parkinsonism is a prominent feature but differs from IPD by associated atypical features.
References-Harrison textbook of Internal medicine,Various sourcres
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 ....
Types of Epilepsy and Choice of Antiepileptics in different SeizuresSawsan Aboul-Fotouh
1- Definition of Epilepsy
2- Types of Epilepsy:
- Partial (Simple and Complex)
- Generalized (Absence, Tonic-Clonic and Myoclonic)
3- Choice of Proper antiepileptic drug in different types of epilepsy
Coma is defined and the anatomy of consciousness explained. The various levels of arousal, AVPU scale and Glasgow Coma Scale described. The differential diagnosis of coma discussed are coma with & without focal deficits and the meningitis syndrome.
The various aspects of history discussed in details. The examination part includes the general examination, Brainstem reflexes, motor functions with the signs of lateralisation and meningeal irritation signs.
The basic lab investigations, Imaging and special investigations like CSF examination, EEG discussed.
Elevated intracranial pressure and its management explained.
Seizures are episodes of abnormal motor, sensory, autonomic, or psychic activity (or a combination of these) resulting from sudden excessive discharge from cerebral neurons.
A seizure is a sudden, uncontrolled electrical disturbance in the brain. It can cause changes in your behavior, movements or feelings, and in levels of consciousness. If you have two or more seizures or a tendency to have recurrent seizures, you have epilepsy.
"The LEW.1WR1 rat is the only model so far that exhibits a low incidence of spontaneous diabetes that can be increased by perturbation. By far the most extensively studied of the models are the two BB rat strains, but all of them have provided interesting information. There are to date no rat models based on the insertion of transgenes, though genetic complementation has been used elegantly to identify the genetic defect in Komeda rats."
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 ....
Types of Epilepsy and Choice of Antiepileptics in different SeizuresSawsan Aboul-Fotouh
1- Definition of Epilepsy
2- Types of Epilepsy:
- Partial (Simple and Complex)
- Generalized (Absence, Tonic-Clonic and Myoclonic)
3- Choice of Proper antiepileptic drug in different types of epilepsy
Coma is defined and the anatomy of consciousness explained. The various levels of arousal, AVPU scale and Glasgow Coma Scale described. The differential diagnosis of coma discussed are coma with & without focal deficits and the meningitis syndrome.
The various aspects of history discussed in details. The examination part includes the general examination, Brainstem reflexes, motor functions with the signs of lateralisation and meningeal irritation signs.
The basic lab investigations, Imaging and special investigations like CSF examination, EEG discussed.
Elevated intracranial pressure and its management explained.
Seizures are episodes of abnormal motor, sensory, autonomic, or psychic activity (or a combination of these) resulting from sudden excessive discharge from cerebral neurons.
A seizure is a sudden, uncontrolled electrical disturbance in the brain. It can cause changes in your behavior, movements or feelings, and in levels of consciousness. If you have two or more seizures or a tendency to have recurrent seizures, you have epilepsy.
"The LEW.1WR1 rat is the only model so far that exhibits a low incidence of spontaneous diabetes that can be increased by perturbation. By far the most extensively studied of the models are the two BB rat strains, but all of them have provided interesting information. There are to date no rat models based on the insertion of transgenes, though genetic complementation has been used elegantly to identify the genetic defect in Komeda rats."
My own slim attempt at covering the extremely complex and ever evolving field of migraine pathophysiology. Not intended by any means to be exhaustive but more like a unique take and beginner's guide.
There are extensive number of neurodegenerative diseases but i have briefly discuss about the eight disease conditions. Hopefully it will be helpful to prospect learner. Good Luck
Derived from Greek word “enkephalos”- meaning brain.
“Pathos” meaning is disease.
The term “encephalopathy” is defined as altered mental status as a result of a diffuse disturbance of brain function.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
2. Seizures
• Definition
– Disorderly excessive discharge of electrical
energy within the neurons of the CNS
• Transient alteration in brain function
– Etiology
• Metabolic disorders: hypoglycemia, hyponatremia
• Hypoxia
• Degenerative disorders
• Infections
• Genetic
• Brain Mass
• Trauma
• Idiopathic
3. Seizures
• Pathophysiology
– Loss of directionality of impulse
– Primary abnormality may be membrane defect
leading to the instability in resting potential,
abnormalities of calcium or potassium, defects
in GABA inhibitory system
– Neurons under electron microscope look bare
with abnormal dendritic processes
4. Seizures
• Seizure initiation
– Firing of abnormal group of neurons will gradually increase in
intensity; threshold reached the discharge can spread through
the cortex, thalamus, and brain stem = TONIC phase
• Muscle contraction with increased tone
• LOC and possible ANS manifestations: brief apnea
– CLONIC phase begins as inhibitory neurons in the cortex,
thalamus, and basal ganglia begin to interrupt the cortical
stimulation
• Alternating contraction and relaxation of muscles
– Increased oxygen and ATP use
• 250% increase in ATP; cerebral oxygen consumption up 60%
• If severe = secondary hypoxia, acidosis (lactic acid)
– Progressive brain injury and destruction
5. Seizures
• Classifications
– Generalized seizures
• Tonic-Clonic (Grand mal)
– Often preceded by an aura
– Abrupt loss of consciousness is followed by tonic
contractions that occur for several seconds
– Alternating contraction/relaxation = tonic-clonic phase
– Neuronal exhaustion with termination of seizure
» Low energy stores
– Stupor or coma for about 5-15 minutes
» Postictal state
– Gradual re-awakening with amnesia of the event
6. Seizures
• Generalized
– Absence (petit mal – old term)
• Occurs in childhood usually after age 4
• Characterized by a brief alternation in
consciousness that can last 5-10 seconds
– Eyes become vacant
– Lips may droop or twitch
• Child immediately resumes activities after seizure
– No postictal state
7. Seizures
• Generalized
– Myoclonic or infantile spasms
• Usually affects children 3 months to 2 years old
– Characterized by flexor spasms of the
extremities and head
• Injury from falling can occur
– Lasts for seconds and can present in clusters
– Usually associated with metabolic,
degenerative, or structural disorders
8. Seizures
• Generalized
– Atonic
• Sudden loss of consciousness
– Individual falls to ground due to loss of postural control
• Partial
– Simple
• Focal motor
– Jacksonian: seizure spreads to adjacent areas after the initial
clonic movement increases
» May begin at finger and move up arm
– Occasionally can have focal motor without Jacksonian march
(progression)
• Focal sensory
– Lesion in the sensory cortex with expression of sensory
changes in the area that is stimulated
» Numbness & tingling of lips, finger, or toes
» Smells or sounds
9. Seizures
• Partial
– Complex
• Temporal lobe
– Impaired consciousness
• Bizarre behavior and exaggerated emotions and
inappropriate verbal responses
– Illusions, hallucinations
• Can interact with environment but may have
inappropriate movements
– May continue to drive or other complex activity
10. Alterations in Cognition
• Data processing defects
– Agnosia
• Failure to recognize form and nature of objects
– Can be tactile, visual, or auditory
• Dysfunction in the primary sensory or interpretive areas of
the cerebral cortex
– Dysphasia
• Impairment in the comprehension or production of language
– Expressive – can’t express thought verbally
– Receptive – can’t understand speech
• Usually due to CVA
– Middle cerebral artery and its branches
11. Alterations in Cognition
• Acute confusional states
– Etiology: associated with delirium and can be caused
by
• Nervous tissue injury
• Toxins exposure
• Drug intoxication
• Metabolic disorders
– Clinical manifestations
• Decreased attention
• Inability to concentrate
• Restlessness
• Poor appetite
• Misperception
• Hallucinations
12. Alterations in Cognition
• Dementia
– Progressive failure of multiple cerebral
functions
– Reduction in intellectual function, decreased
orientation, recent memory loss, decreased
language function, change in behavior
– Etiology: trauma, vascular disorders,
infections, and Alzheimer’s Dz
• Vascular – Lewy Bodies, Lacunar infarcts
13. Alterations in Cognition
• Dementia
– Pathophysiology
• Multiple infarcts with actual destruction of cortical
tissue
• Decrease in NT Acetylcholine with abnormalities in
amyloid production and deposition
• See table 16-18 on page 553
14. Alzheimer’s Disease
• Severe cognitive dysfunction
– Etiology:
• Loss of neurotransmitter stimulation by choline
acetyltransferase
• Mutation of encoding amyloid precursor protein
• Abnormalities in apolipoprotein E (apoE4) which
binds amyloid-beta
• Excessive influx of calcium due to abnormal
activation of N-methyl – D – aspartate receptors
• Other chromosomal abnormalities linked to early
and late onset FAD
15. Alzheimer’s Disease -
pathogenesis
• Each of the etiologies are
linked to the aggregation and
precipitation of insoluble
amyloid in the form of plaques
in brain tissue and blood
vessels
• There may be a lysosomal
breakdown of amyloid where
beta amyloid, a neurotoxin, is
the end product
• It is thought once amyloid
plaques form, complement
proteins attach and attract
microglia
– Release toxins to try to
destroy the plaque
• Tau proteins detach from
microtubules and form
neurofibrillary tangles
16. Alzheimer’s Disease
• Clinical manifestations
– Forgetfulness
– Loss of recent memory
– Loss of attention
– Decreased abstract
thinking
– Decreased cognitive and
intellectual function
– Irritability, confusion,
disorientation
– Mood swings
17. Cerebral Hemodynamics
• Definitions
– Cerebral blood volume (CBV): amount of
blood in cranial vault. 10%
– Cerebral blood flow (CBF): controlled by
localized metabolic needs associated with
changes in O2 and CO2
• 15-20% of cardiac output
– Cerebral perfusion pressure (CPP): pressure
required to perfuse cerebral cortical cells
• CPP = MAP - ICP
18. Cerebral Hemodynamics
• Intracranial pressure (ICP)
– Normal value 5-15 mm Hg
– Increasing ICP etiology:
• Increased content (brain mass)
• Increased interstitial fluid (cerebral edema)
• hemorrhage
• Increased CSF
– Pathophysiology
• When there is a change in one of the above there will be an
increase in ICP
• Adaptation:
– Initially the body will decrease the CSF in order to keep ICP in
normal range
19. Cerebral Hemodynamics
• Increasing ICP
– Adaptive responses
• If decreasing the CSF is not effective
– Vasoconstriction of the vasculature and external
compression of the venous system to decrease in ICP
– Increased vasoconstriction will cause stage 1 intracranial
HTN but there will not be an increase in ICP if the
adaptation is effective
– As ICP reaches MAP there will be a marked reduction in
cerebral blood flow and increased hypoxia
– Systemic HTN will occur in order to continue to perfuse
the brain during high ICP
20. Cerebral Hemodynamics
• Increasing ICP continues
– When compensatory mechanisms of reabsorbed CSF,
vasoconstriction of cerebral arteries, venous
compression, and increased SBP fails:
• ICP: dramatic rise in short time period; ICP > MAP
– Marked hypoxia will increase inflammation = increased cerebral
edema = marked deterioration in the patient’s condition
– Brain tissue will shift and herniate under or through bony
structures within the skull:
» Falx cerebri, tentorium, tentorial notch, foramen magnum
– Coma and death
21. Cerebral Hemodynamics
• Cerebral edema
– Definition: increased fluid content in the brain
– Types
• Vasogenic – increased permeability of the capillary
endothelium after injury to the vascular structure
with disruption of the blood brain barrier
– Leakage of plasma proteins into interstitial tissue
» Increased water content in the parenchyma = edema
– Increased edema = increased hypoxia = increased
edema cycle (white matter)
22. Cerebral Hemodynamics
• Cerebral edema
– Types (cont.)
• Cytotoxic (metabolic) – toxic factors directed affect
cellular elements of neuronal, glial, or endothelial
cells with failure of active transport systems,
– Blood brain barrier is intact
– Failure of the Na-K ATPase pump
» Cells will lose K and gain a lot of Na
» Water follows by osmosis
» Cells swell (primarily gray matter)
– May increase vasogenic edema
23. Cerebral Hemodynamics
• Cerebral edema
– Types (cont.)
– Ischemic – cerebral infarction
• Release of lysosomal enzymes with destruction of cells
– Initiates both vasogenic and cytotoxic mechanisms
» Increased membrane permeability and active transport
failure
– Interstitial – associated with hydrocephalus
• Increased amount of CSF
– Ependymal cells moves CSF from ventricles to extracellular
spaces of the brain tissue
» Hydrostatic pressure in white matter around the ventricles
increase
25. Traumatic Brain Injury
• Types of TBI:
– Blunt (closed) trauma: head striking hard
surface or rapidly moving object
• Dura mater remains intact
– Open (penetrating) trauma: mechanism of
injury may be the same but there is a break in
the dura mater
• Brain tissue exposed to environment
26. Traumatic Brain Injury
• Definitions:
– Coup injury: injury directly below the area of trauma
– Contrecoup: occurs on the opposite side of the injury
– Focal brain injury: specific grossly observable brain
lesion with:
• Cortical contusions
• Epidural hemorrhage
• Subdural hematoma
• Intracerebral hematoma
– Diffuse axonal injury (DAI): diffuse injury due to
acceleration/deceleration
• Brain experiences shearing, tearing, or stretching of nerve
fibers
28. Traumatic Brain Injury
• Focal brain injury
– Pathophysiology: force of impact produces
contusions due to the compression of the skull
at the point of impact and a rebound effect
– Contusion is associated with hemorrhage,
infarction, cerebral edema, and increasing
ICP
29. Traumatic Brain Injury
• Focal brain injury
– Associated bleeding can cause:
• Epidural hematomas – arterial bleeding between the dura
mater and skull
– Most common arterial tear is in the middle meningeal artery
» Lateral shift and uncal herniation
• Subdural hematoma – venous bleeding into the subdural
space; acute or chronic presentations
– Increase ICP
• Intracerebral hematoma – injury to smaller vessel within the
brain
– Hematoma acts like expanding mass with increasing ICP
30. Traumatic Brain Injury
• Focal brain injury
– Clinical manifestations
• Immediate loss of consciousness
– No longer than 5 minutes
• Brief period of bradycardia, decreased BP
• Epidural hematoma Hx: period of LOC followed by
period of lucidity and potential for rapid
deterioration depending on level of this arterial
bleeding
• Subdural hematoma Hx: HA, drowsiness,
restlessness, agitation, slowed cognition, and
confusion which can progress to herniation
32. Traumatic Brain Injury
• Diffuse brain injury
– Etiology
• Usually results for shaking, rotational effect, high levels of
acceleration and deceleration
– Causes shearing, tearing, stretching of axons
» Most common in the frontal and temporal axonal tracts
• Diffuse brain injury
– Types
• Mild concussion: temporary interruption in axonal function
resulting in memory loss and confusion
• Classic cerebral contusion: diffuse cerebral disconnections
that result from neurological dysfunction without anatomical
disruption.
– LOC up to 6 hours
33. Traumatic Brain Injury
• Diffuse brain injury
– Types (cont.)
• Mild DAI: posttraumatic coma lasting 6-24 hours
with resultant cognitive, psychological, and
sensorimotor deficits
• Moderate DAI: widespread disruption with actual
tearing of some axons. Prolonged coma > 24
hours with incomplete recovery
• Severe DAI: major brain stem and axonal damage
associated with prolonged coma if patient survives
36. Cerebrovascular
Disorders
• Types of strokes
– Thrombotic Stroke:
• Arterial occlusion caused by thrombi formed in
the vessels supplying the brain or in the
intracranial vessels
• Etiology
– Atherosclerosis
– Inflammation as in arteritis
– Increased coagulation
– Decreased cerebral blood flow
37. Cerebrovascular
Disorders
• Thrombotic Strokes
– TIA: transient ischemic attacks caused by an
intermittent blockage of vessel or spasm
causing clinical manifestations that clear
within 24 hours
– Stroke in evolution: intermittent progression
of clinical manifestations over hours or days
– Completed stroke: Stroke has reached
maximum destructiveness
38. Cerebrovascular
Disorders
• Embolic Stroke
– Fragments that break from a thrombus
formed outside of the brain (examples heart,
aorta, common carotid)
– Risk factors
• Atrial fibrillation
• Endocarditis
• Valve prosthesis
• Fat emboli secondary to long bone fractures
39. Cerebrovascular
Disorders
• Hemorrhagic Stroke
– Risk factors
• Hypertension
• Malformations of cerebral vasculature
• Bleeding into a tumor
• Anti-coagulation
• Lacunar Stroke
– Micro-infarcts that involve the small
perforating arteries that are associated with
hypertension and diabetes
40. Cerebrovascular
Disorders
• Cerebral Infarction
– Pathophysiology
• Infarction is associated with hypoxia of tissues
and the following cellular events:
– Altered cell membranes with influx of calcium, failure
of the mitochondria, alterations in the sodium and
potassium pump function, cerebral edema, with fall in
pH
– Cerebral edema reaches it maximum at 72 hours
– Clinical manifestations are dependent upon the
localization of the stroke
– See Table 17-6 page 604-605
41. Cerebrovascular
Disorders
• Intra-cranial Aneurysms
– Definition: weakness in the vessel wall
• Etiology
– Congenital malformation
– Arteriosclerosis
– TraumaInfection
– Cocaine use
• Types:
– Saccular: gradual growth over time of sac in the vessel
walls
– Fusiform: greater than 25 mm and result from diffuse
arteriosclerosis. Commonly found in the basilar arteries or
terminal internal carotids
42. Aneurysm
• Intracranial Aneurysms
No Clinical manifestations
– until they rupture or
increase in size and put
pressure on surrounding
brain structures
43. Cerebrovascular
Disorders
• Subarachnoid.Hemorrhage
– Definition: bleeding into the subarachnoid space
– Risk factors
• Hypertension
• AV Malformations
• Trauma
– Pathophysiology
• Blood enters the subarachnoid space, increases inflammation,
impairs cerebral spinal fluid reabsorption, increases intracranial
pressure with a decrease in cerebral perfusion pressure
– Clinical manifestations:
• Ruptured vessel with severe, throbbing explosive headache, n/v,
motor deficits, and loss of consciousness
• Increased ICP, meningeal irritation
45. Cerebrovascular
Disorders
• Vascular Malformations
– Types:
• Arteriovenous malformations: arteries feed
directly into veins through a tangle of malformed
vessels. Increased incidence of bleeding
• Cavernous Angiomas: sinusoidal collections of
blood vessels without brain tissue interspersed.
Rarely bleed
• Capillary telangiectasis: dilated capillaries
with interspersed normal brain tissue. Bleed
only rarely and are associated with Rendu-
Oster-Weber disease
46. • Put picture of AV malformation here – try
to find all three types
48. Headache
• Migraine
– Pathophysiology
• Theories
– Vascular theory: abnormalities in cerebral blood flow with
vasoconstriction during the during the aura phase and
vasodilatation during the headache phase. Blood flow is
impaired but research does not support a reduction that
could be responsible for the development of the common
clinical manifestations
– Cortical spreading depression: reduction in brain and
electrical activity with depressed blood flow, release of
potassium and hydrogen ions with stimulation of sensory
neurons
49. Migraine Headache
• Pathophysiology
– Theories
• Serotonergic and neurotransmitter alteration
– Increased release of serotonin, norepi, subst P that activates
neurotransmissions to the cerebral arteries
» Altering blood flow
» Increased inflammation
– Phases
• Trigger phase
• Aura with inhibition of cortical activity and reduction in blood
flow
• Release of vasoactive neuropeptides, ionic alterations,
platelet release of serotonin, and degranulation of mast cells
• Activation of the locus ceruleus and excitation of the
trigeminal nuclei resulting in dilation of dural arteries
50. Headache
• Cluster Headaches
– Etiology/Pathophysiology
• Unknown
– Clinical Manifestations
• Lacrimation
• Reddening of the eye
• Nasal stuffiness
• Eyelid ptosis
• Nausea and vomiting
• Pain referred to midface and teeth
51. Headache
• Tension
– Pathophysiology
• Central mechanism: involves hypersensitivity of
the pain fibers from the trigeminal nerve with
increased pain
• Peripheral mechanism: related to contraction of
the jaw and neck muscles
• Likely occurs on a continuum with migraine
headaches and most people will have both at
one time or another
52. CNS Infections
• Meningitis
– Definition: infection of the meninges that can
be caused by bacteria, fungi, viruses, or
parasites
– Bacterial:
• Most common causes:
– Pneumococcus (Strep pneumoniae)
– Meningococcus (Neisseria meningitdis)
• Most common spread is by blood stream from
the extracranial site of infection
53. CNS Infections
• Meningitis
– Viral
• Infection that is most likely limited to the meninges
• Can be caused by all of the common upper respiratory
viruses
– Fungal
• More insidious in its onset and occurs most often in
individuals who are immunocompromised
• Infection with coccidiomycosis, histoplasmosis,
cryptococcosis are the most common
• Tuberculosis
– Increased in immunocompromised individuals
54. CNS Infections
• Pathophysiology
– Entry of the bacteria through the choroid plexus
– Toxins stimulate inflammatory response
– Increased permeability of the meningeal vessels with
movement of white blood cells into the subarachnoid
space
– Exudate production with potential for obstruction of
arachnoid villi and the production of hydrocephalus
– Edema of tissue with increased intracranial pressure
– Fungi can also cause the formation of granulomas,
arteritis, thrombosis, and hydrocephalus
57. Degenerative
Neurological Diseases
• Parkinson‘s
– Degenerative disease of the basal ganglia involving
the dopaminergic neurons (substantia nigra and
others)
– Types
• Primary: idiopathic
• Secondary: impact of toxins, drugs, infection
– Pathophysiology
• Cerebral atrophy and neuronal loss
• Degeneration of the dopaminergic neurons of the
nigrostriatal pathway
• Lewy bodies and intracytoplasmic eosinophila inclusion
bodies are found in the neurons that have not been
destroyed
58. Degenerative
Neurological Diseases
• Parkinson‘s Disease
– Pathophysiology
• Depletion of dopamine which is a inhibitory
neurotransmitter is responsible for the
development of the typical clinical
manifestations
• Imbalance of dopaminergic (inhibitory) and
cholinergic (excitatory) activity which is
responsible for the hypertonia and akinesia
59. Degenerative
Neurological Diseases
• Parkinson's Disease
– Clinical Manifestations
• Resting tremor
• Rigidity
• Akinesia
• Bradykinesia
• Postural Abnormalities:
– Involuntary flexion of the head and neck
– Shuffling gait secondary to disorders in equilibrium
– Difficulty in maintaining balance or righting when balance is
lost
• Depression
• Dementia
• Bradyphrenia
60. Degenerative
Neurological Diseases
• Multiple Sclerosis
– Progressive demyelinating disease of the central
nervous
system
• Etiology: viral insult in a genetically susceptible
individual causes an increased immune response with an
immunogenic destruction of the myelin
– Pathophysiology
• Immune system response to environmental challenge
• Immune cells arriving at the myelin sheath excrete glutamate
which is then ingested by oligodendrocytes
• Plaques and diffuse CNS lesions produce slowing of
conduction initially with a progressive conduction block
• Glial scarring with degenerations of axons
61. Degenerative
Neurological Diseases
• Multiple Sclerosis
– Types by classifications:
• Relapsing Remitting: characterized by distinct periods of
Improvement and acute attacks
• Primary Progressive: steady worsening of symptoms
from the beginning
• Secondary Progressive: begins with periods of
remission and relapses but becomes steadily more
progressive
• Progressive Relapsing: steadily progressive but has
periods of acute attacks as well
62. Degenerative
Neurological Diseases
• Multiple Sclerosis
– Clinical Manifestations (Syndromes)
• Spinal type: spastic ataxia, deep sensory changes
in the extremities, and bowel and bladder
symptoms, weakness and numbness
• Cerebellar: motor ataxia, hypotonia, asthenia,
nystagmus
• Mixed: optic neuritis, diplopia, vertigo, cerebellar
signs, visual field defects,
64. Degenerative
Neurological Diseases
• Amyotrophic Lateral Sclerosis
– Involves upper and lower motor neuron degeneration
– Predominant lower motor neuron dysfunction in the
early stages
– Usually begins in one muscle group
– Lower motor neuron symptoms
• Flaccid paralysis
• Hypoactive reflexes
• Atrophy
• Fasciculations
65. Degenerative Neurological Diseases
• Amyotrophic Lateral Sclerosis
– Upper motor neuron syndromes
– Spastic paresis
– Atrophy
– Hyperactive deep tendon reflexes
– Clonus
– Clinical manifestations
• Progressive muscle weakness
– Paresis begins in one muscle group
– Muscle groups – asymmetrically affects
– Gradually affects all striated muscles
» Exceptions: extraocular and heart
– Spastic paresis may be masked by flaccid paresis
66. CNS Tumors
• Primary
– Astrocytomas
• most common tumor that grows by expansion and
infiltration, located within the cerebellum
– Most common lobes: frontal, temporal, and parietal
– Gradual growth and increase in ICP
– Often found initially with the onset of a new seizure
– Oligodendrogliomas
• less common tumor that is slow growing and found
in the frontal lobe
– Ependymomas
• arise from the fourth ventricle
Increased incidence in children
68. Diseases of the Neuromuscular
Junction
• Myasthenia Gravis
– Etiology: autoimmune disease mediated by the anti-
acetylcholine receptor antibodies that act at the
neuromuscular junction
– Pathophysiology
• Defect in nerve impulse transmission at the neuromuscular
junction
• Post synaptic receptors on the muscle cell membrane are
selectively destroyed by the immune system production of
receptor antibodies
• Decreased receptor sites, decreases the effectiveness
of ACH at the neuromuscular junction, with slowing of
transmission
69. Diseases of the Neuromuscular
Junction
• Myasthenia Gravis
– Clinical Manifestations
• Insidious onset
• Fatigue and weakness with increased symptoms
after exercise
• Diplopia, ptosis, ocular palsies
• facial droop, difficulty swallowing, weight loss
• Respiratory depression, increasing weakness of
the legs and arm muscles (proximal)