The document provides guidance on performing a neurological examination on a patient presenting with coma. It describes assessing the level of consciousness using the AVPU and Glasgow Coma scales. Key aspects of the physical exam are outlined, including vital signs, signs of trauma, skin appearance, neck stiffness, pupil size/reactivity, and posture responses that may indicate lesions in specific areas of the brain or brainstem. Priority is given to the ABCs to ensure adequate oxygenation and circulation as underlying life-threatening conditions are addressed first before a more thorough neurological assessment.
Subarachnoid hemorrhage a major complication ,this presentation can help you understand the disease, the signs & symptoms and give you the diagnostic feature ,I hope you well enjoy studying it ... Good luck :)
70% of RTA patients have head injury(HI).
One of the most important public health problems of today.
70% of deaths in RTA are due to HI.
At Risk population
Males 15-24
Infants
Young Children
Elderly
Subarachnoid hemorrhage a major complication ,this presentation can help you understand the disease, the signs & symptoms and give you the diagnostic feature ,I hope you well enjoy studying it ... Good luck :)
70% of RTA patients have head injury(HI).
One of the most important public health problems of today.
70% of deaths in RTA are due to HI.
At Risk population
Males 15-24
Infants
Young Children
Elderly
INITIAL ASSESSMENT OF TRAUMA PATIENTS....(INSPIRED FROM CTLS AND ATLS GUIDELI...Prerna Biswal
THIS PRESENTATION WAS MADE AT IMA HOUSE IN BHUBANESWAR,ODISHA, BY DR.NIBEDITA PANI,HOD ,DEPT. OF ANAESTHESIOLOGY AND DR.PRERNA BISWAL,PG,ANAESTHESIOLOGY,SCBMCH,CUTTACK,
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.
Approach to coma
1-Definition
2-Pathophysiology, Causes, and similar condition
3-History and general physical examination
4-Neurological examination
5-Investigation
6-Management
A brief presentation about confusional states. Difference between coma. This presentation is focused on Pathophysiology, major causes and approach to diagnosis and diagnosis tools.
#Altered level of consciousness is a common condition in #pediatrics that must have urgent #treatment to avoid serious #complications on the baby. this presentation will show the #definition, #etiology ( #causes), clinical #signs & #symptoms, #differential diagnosis, and #treatment of #altered_level of consciousness #Aloc (#aloc).
https://www.slideshare.net/mero92/
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
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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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
2. HISTORY
Wherever possible an account of events
preceding coma should be obtained directly
from witnesses as family , friends , from
ambulance personnel or physicians that
treated the patient before that’s helpful for
know the cause then taking correct diagnosis
Is the PT had MNMPsIreuneeeurjddvugriicriooccealauaodtllsi g oi (ilipltlnclnrnsasuyee lma csschnssoaeeodn)ssl dor??eigtciicroeanals t ci?oonnadli tdiorung?s ?
DME ,p ailsetphsmyD a,en, pehruyerpsoessiroutenrgnesrioFyAn L ,ScEa nCcOeMr A
Ask them about recent complaints as ,headache , head
injury(Don’t move spine until the neurologist see pt),
dizziness/vertigo ,seizures, tremors , weakness .
3. WHAT last time was the patient look alter and conscious ?
The possible diagnosis are Influenced by the rate of onset of coma
Cerebrovascular
episodes,drug abuse
hypoglycemia
Fulminating infection
post-ictal condition
Developed
Suddenly
Kitoacidosis
Chronic renal failure
Hepatic dysfunction
Insidious
In onset
mode of onset
•Subarachnoid
hemorrhage
• brainstem stroke
• intracerebral
hemorrhage
HISTORY
4. Priorities
•ABC’s are Paramount !
Airway : any sign of obstruction ? ascertain patency .
Breathing :RR, rhythm ,check bilateral chest movement ,percuss and
•Clinical Examination: Quick and precise.
•Rapid and appropriate investigations: To find
cause and institute appropriate
treatment.
auscultate.
Circulation :Pulse rate,rhythm . volume BP , evidence of haemorrhage
Cushing`s response ( BP with slow Pulse )occur in response to sever
ICP and signs of Cerebral Herniation .
•Must ensure oxygen and substrate reach CNS and vital organs .
•Must address immediately life threatening conditions before
addressing CNS .
Immediat treatment of these life threatening conditions before doing
farther clinical examination
5. GENERAL PHYSICAL EXAMINATION
Skin :
•Injuries, Bruises: traumatic causes
•Dry Skin: DKA, Atropine
•Moist skin: Hypoglycemic coma
•Cherry-red: CO poisoning
•Needle marks: drug addiction or SC insulin injection
•Rashes: meningitis , hypersensitivity , endocarditis
•Color : cyanosis, pallor
•cutaneous petechiae: Thrombotic
thrompocytopenic prupra,
meningococcemia,or
bleeding diathesis(Intracerebral heamorrhage).
6. GENERAL PHYSICAL EXAMINATION
• Head examination:
Depressed skull
fracture .
Bruising over mastoid
process .
Battle`s sign
Racoon eyes
CSF or blood
discharge from nose
or ear.
Palpation of the
orbital margins
Middle fossa fracture
Anterior cranial fossa fracture
LIFE THREATENING
Basilar skull fracture
Zygomatic or malar
fracture
7. GENERAL PHYSICAL EXAMINATION
• Temperature:
I-Hypothermia: causes coma only when the temperature is
<31°C
• Hypopituitarism
• Hypothyroidism
• Chlorpromazine
• Hypoglycemia
• Peripheral circulatory failure
• Alcoholic ,barbiturate , sedative, phenothiazine intoxication
• Exposure to low temperature environments, cold-water immersion
Risk of hypothermia in the elderly with inadequately heated rooms ,
exacerbated by immobility.
all vital signs may be decreased(or absent) and all such patients should be
gradual rewarmed before the prognosis is assessed.
8. GENERAL PHYSICAL EXAMINATION
• Temperature:
II-Hyperthermia (febrile Coma)
• Infective: encephalitis, meningitis
• Vascular: pontine, subarachnoid hge
• Metabolic: thyrotoxic, Addisonian crisis
• Toxic: belladonna, salicylate poisoning
• Sun stroke, heat stroke
• Coma with 2ry infection: UTI, pneumonia, bed sores.
• Only rarely is it attributable to a brain lesion that has
disturbed temperature-regulating centers as Lesions in
the floor of the third ventricle ,Neuroleptic malignant
syndrome.
•High fever(42-44°C)
associated with dry skin
should arouse the
suspicion of heat stroke or
anticholinergic drug
intoxication.
Other causes
•Tetanus
•Malignant hyperpyrexia with anaesthetics.
10. GENERAL PHYSICAL EXAMINATION
• Neck stiffness
– infection, trauma, or subarachnoid bleeding.
– (Do not manipulate the neck if there is suspicion of cervical
spine fracture.)
• Chest, abdomen, heart, and extremities
Must be examined routinely. Rectal and pelvic examinations plus a
stool test for blood should also be performed.
• Fundoscopic examination
Subarachinoid hemorrhage(subhyaloid hemorrhage).
Hypertensive encephalopathy (exudate, hemorrhage ,
vessel-crossing changes, papilledema).
Increase ICP (papilledema).
11. •Vital signs are vital-obtain full set, including temperature.
•Signs of trauma ”haematoma, laceration, bruising, CSF/blood in nose or ears, fracture ,step
deformity of skull, subcutaneous emphysema, panda eyes.
•Stigmata of other illnesses: liver disease, alcoholism, diabetes, myxoedema .
•Skin for needle marks, cyanosis, pallor, rashes, poor turgor.
•Smell the breath (alcohol, hepatic fetor, ketosis, uraemia).
•Meningism but do not move neck unless cervical spine is cleared.
•Pupils size, reactivity, gaze.
•Heart/lung exam for murmurs, rubs, wheeze, consolidation, collapse.
•Abdomen/rectal for organomegaly, ascites, bruising, peritonism, melaena.
•Are there any foci of infection (abscesses, bites, middle ear infection?)
•Any features of meningitis: neck stiffness, rash, focal neurology?
•Note the absence of signs, eg no pin-point pupils in a known heroin addict.
12. NEUROLOGIC
EXAMINATION
DERM
D = Depth of Coma
E = Eyes
R = Respiratory Pattern
M = Motor Function
13. Observation first without examiner intervention.
wallowing
reach up toward the face
cross their legs
yawn
Swallow
cough
moan
Awake(light coma).
Lack of restless movements on one side
an out turned leg at rest Hemiplegia.
Multifocal Myoclonus metabolic disorder
drowsy and confused
patient with bilateral
asterixis
Metabolic
encephalopathy
Drug ingestion.
Jaw and lid tone also indicates the severity of unconsciousness.
Open lids and hanging jaw bespeak deep coma.
14. Decorticate posture
This posture is noted
from lesion of the
cortex and basal
ganglion.
The patient has
•Flexed arms
•Extended legs and
• Internally rotated
feet.
•Associated with 2–3
mm pupils that react
to light and periodic
reaction.
Decorticate posture. Note the eyes are conjugately deviated to the side of the lesion.
15. Decerebrate rigidity
•Commonly from
Structural Brainstem
damage.
However,
hypoglycemia,
hepatic failure,
hypoxia and
phenobarbital
intoxication
cause reversible
decerebration.
•arms Adducted extended
•Wrist pronated and the fingers flexed
•Legs are stiffly extended with planter flextion of the feet
16. Decerebrate posture Decorticate posture
Both decorticate and decerebrate postures are elicited by
painful compression of the supraorbital nerve or sternum.
17.
18. Parietal lobe.
Note that the patient lies across the bed such that there is neglect of
the left side of space.
The patient denies the left side of space. He or she will be found on
the right side of bed at an angle (the feet more toward the midline). If
the lesion is in the thalamus there is profound loss of position sense
and the patient will be lying on the arm in a very awkward position.
19. Corticospinal posture
The head and eyes are deviated to the left hemispheric lesion. The
right arm is pronated with an adducted thumb. The left arm is
supinated with an adducted thumb. The right leg is externally rotated.
20. Brainstem hemiparetic posture.
The head and eyes are deviated to the right, the same side as the
hemiparesis as noted from the adducted thumb
21. Bilateral corticospinal stroke
The eyes are deviated to the right and the right arm is pronated with
an adducted thumb. The lesion is at the level of the left parapontine
reticular formation. The left arm is pronated and the left foot
externally rotated as a result of the brainstem corticospinal
involvement. If the patient were “locked in”, the eyes would be
midline.
22. Bifrontal posture
•Usually of long-standing.
•Flexed arms and legs.
• Apraxia of swallowing may be seen. It may appear as
fetal posture with both arms and legs flexed
23. Degrees of wakefullness
Alert= awake
Awake, confused, disoriented
Lethargic: easily aroused with speech or touch
Obtunded: mild to moderate loss of arousability. Falls
asleep unless verbally or tactile stimulation
Stupor: deep sleep or unresponsive. Responds to deep
painfull stimulation
Coma: no verbal response, motor responses may be to deep
painful stimulation
To assesses a patient level of unconsciousness
• AVPU
• Glasgow Scale (GCS)
24.
25. The AVPU scale
(Alert, Voice, Pain, Unresponsive) is a system by which a first aider, ambulance crew or health
care professional(or as we just student) can measure and record a patient's responsiveness,
indicating their level of consciousness.
•Alert - a fully awake (although not necessarily orientated) patient. This patient will have
spontaneously open eyes, will respond to voice (although may be confused) and will have
bodily motor function.
In some EMS protocols, "Alert" can be subdivided into a scale of 1 to 4, in which 1, 2, 3 and 4
correspond to certain attributes, such as time, person, place, and event.
•Voice - the patient makes some kind of response when you talk to them, which could be in any of
the three component measures of Eyes, Voice or Motor - e.g. patient's eyes open on being
asked "are you okay?!". The response could be as little as a grunt, moan, or slight move of a limb
when prompted by the voice of the examinor .
Pain – its done if the patient don’t responde to the upper tow methodes :
Sternal rub the rescuers knuckles are firmly rubbed on the breastbone of the patient.
pinching the ear of the patient's and pressing a pen into the bed of the patient's fingernail.
A fully conscious patient would normally locate the pain and push it away
Patient who is not alert likely to exhibit only withdrawal from pain, or even involuntary
flexion or extension of the limbs from the pain stimulus.
Ambulance crews may begin with an AVPU assessment, to be followed by a GCS assessment if
the AVPU score is below "A."
26. Glasgow Coma Scale
The scale was published in 1974 by Graham Teasdale and Bryan J. Jennett, professors
of neurosurgery at the University of Glasgow's Institute of Neurological Sciences at
the city's Southern General Hospital.
oSevere, with GCS ≤ 8
oModerate, GCS 9 - 12
oMinor, GCS ≥ 13.
The score is expressed in the form "GCS 9 = E2 V4 M3 at 07:35"
Tracheal intubation and severe facial/eye swelling or damage make it
impossible to test the verbal and eye responses. In these circumstances, the
score is given as 1 with a modifier attached e.g. 'E1c' where 'c' = closed, or 'V1t'
where t = tube. A composite might be 'GCS 5tc'. This would mean, for example,
eyes closed because of swelling = 1, intubated = 1, leaving a motor score of 3
for 'abnormal flexion'. Often the 1 is left out, so the scale reads Ec or Vt.
Don’t
Miss
27. eye response (E)
1.No eye opening
2. Eye opening in response to pain. (Patient
responds to pressure on the patient’s
fingernail bed; if this does not elicit a
response, supraorbital and sternal pressure
or rub may be used.)
3. Eye opening to speech. (Not to be confused
with an awaking of a sleeping person; such
patients receive a score of 4, not 3.)
4. Eyes opening spontaneously
Best verbal response (V)
There are 5 grades starting with the most severe:
1.No verbal response
2.Incomprehensible sounds. (Moaning but no words.)
3.Inappropriate words. (Random or exclamatory
articulated speech, but no conversational exchange)
4.Confused. (The patient responds to questions
coherently but there is some disorientation and
confusion.)
5. Oriented. (Patient responds coherently and
appropriately to questions such as the patient’s
name and age, where they are and why, the year,
month, etc.)
Best motor response (M)
There are 6 grades starting with the most severe:
1.No motor response
2.Extension to pain (adduction of arm, internal rotation of shoulder, pronation of forearm,
extension of wrist, decerebrate response)
3.Abnormal flexion to pain (adduction of arm, internal rotation of shoulder, pronation of
forearm, flexion of wrist, decorticate response)
4.Flexion/Withdrawal to pain (flexion of elbow, supination of forearm, flexion of wrist when
supra-orbital pressure applied ; pulls part of body away when nailbed pinched)
5.Localizes to pain. (Purposeful movements towards painful stimuli; e.g., hand crosses mid-line
and gets above clavicle when supra-orbital pressure applied.)
6.Obeys commands. (The patient does simple things as asked.)
28. Revised Trauma Score
The reasoning is that diverting scarce resources away from people with a little chance of survival increases the
chances of survival of others who are inherently more likely to survive.
•The score range is 0-12.
•A patient with an RTS score of 12 is labeled DELAYED (walking
wounded)
• 11 is URGENT (intervention is required but the patient can wait a short
time)
• 10-3 is IMMEDIATE (immediate intervention is necessary).
•The last possible label is MORGUE which is given to seriously injured
people with an RTS score of 3 or lower. These people should not receive
certain care because they are unlikely to survive.
GCS score + Respiratory score + Systolic BP score =
Revised Trauma Score
30. Pupillary Changes
• Size, equality, and roundness of pupils assessed
• Size measured in millimeters
• Evaluated for symmetry in size and response to
light stimulus
• Brisk, sluggish, non-reactive
• Oculomotor response (Cranial nerve III)
• Consensual reaction of opposite pupil at same
time
31. Pupillary Changes to Light
• Assess accommodation by holding finger 4-6 inches from client’s
nose and then pull out to 18 inches.
• As finger moves away pupil will accommodate by dilating, as
finger moves closer, constricting
• PEARLA- Pupils Equal and Reactive to light and Accommodation
32.
33. Pupils
As a general rule: most metabolic encephalopathies give small pupils
with preserved light reflex.
Atropine, and cerebral anoxia tend to dilate the pupils, and opiates
and OPC will constrict them.
A unilaterally dilated and unreactive pupil in a comatose patient
(Hutchinson pupil)
may be a sign of third nerve compression due to temporal lobe
herniation.
Small but reactive pupils signify pontine damage, as in infarction or
hemorrhage.
Opiates and pilocarpine also produce pinpoint reactive pupils.
Dilatation of the pupils in response to a painful stimulus in
the neck (the normal ciliospinal reflex) indicates lower
brainstem integrity.
34. pontine damage
compression of the III
nerve (coning of the
temporal lobe uncus).
This is a potential
neurosurgical
emergency (e.g.
extradural haematoma). Lightfixed pupils (4–6 mm), sometimes
irregular, are seen in brainstem lesions.
cardinal sign of brain
death. They can occur
in deep coma of any
cause, but particularly
in barbiturate
intoxication and
hypothermia
Pontine lesions
(e.g. haemorrhage
and with opiates).
metabolic comas and follow coma due to
sedative drugs except opiates
35. Eye movements
Spontaneous roving, horizontal and conjugate eye movements
intact brain stem
diffuse or metabolic cortical dysfunction
Conjugate lateral deviation
massive hemispheric lesion (eyes toward lesion)
pontine lesion (eyes away from lesion)
Doll’s eyes reflex
intact brainstem function with depressed cortical influences
normal sleep, coma, persistent vegetative state
Ice water caloric test
eyes toward the side of cold water
absence in brainstem lesion, inner ear disease, deep drug coma, and anticonvulsants
overdose
38. Doll’s-head maneuver
•Called oculocephalic
reflex
•to confirmed that there
is no tympanic rupture
•Passive head turning
produces conjugate
ocular deviation
away from the direction
of rotation.
•This reflex disappears in deep coma, in brainstem lesions
and in brain death or C-spine injury.
39. Calledoculovistibular reflex
• Used in the confirmation of brain death.
• Slow tonic ocular deviation towards the
irrigated ear(nystagmus) is seen when
ice-cold water is run into the external
auditory meatus –caloric/vestibulo-ocular
reflexes, indicating an intact
brainstem.
Ice water calorics test
40.
41. Motor responses
may be spontaneous, induced, or reflexive.
A- Spontaneous
• Seizures may be
– focal, in which case they have some localizing value.
– Generalized seizures do not help in localizing the lesion
– Multifocal seizures are suggestive of a metabolic process.
• Myoclonic jerks also point to metabolic encephalopathies (e.g.,
hypoxia, hepatic failure uremia).
• Asterixis has the same significance.
• Absence of movements on one side of the body, or asymmetry of
movements, suggests hemiparesis.
42. Motor responses
B. Induced movements
– (e.g., fending-off or other complex, purposeful
movements, such as scratching the nose in response to
tickling of the nostril) require integrity of the
corresponding corticospinal tract.
– Poorly organized, incomplete movements, especially when
unilateral, suggests corticospinal tract dysfunction or
damage.
44. Pattern causes Description
Cheyne-Stokes • bilateral deep hemispheric and
basal ganglionic dysfunction.
•± upper brainstem involvement.
•congestive heart failure
Hyperventilation and
hypoventilation with pauses.
Central
Neurogenic
Hyperventilation
(kussmauls)
Systemic acidosis (e.g., diabetic
ketoacidosis, lactic acidosis) and
hypoxemia should be excluded
Rapid, deep breathing
Apneustic
breathing
pontine damage. Prolonged inspiratory gasp
followed
by a pause and then expiration
Cluster breathing High medullary lesions Periodic breathing with irregular
frequency
and amplitude, along with
variable pauses
Ataxic breathing Imply damageto the medullary
respiratory centers. Both are
agonal events and usually
precede respiratory arrest
Irregular in rate and rhythm
45. Thank you for your attention
Thank you for
saving me
from coma