Neurology Lectures: Key Dates and Topics

Important Dates and Lectures

• January 13, 2025: No classes are scheduled
• January 20, 2025: Orientation day
• January 27, 2025: Neurologic Examination and Approach to Neurologic Diagnosis and Increased Intracranial Pressure and BBB (NE and Approach), 30 minutes
• February 3, 2025: Neuro-Diagnostic Evaluation and ICP and BBB, 25 minutes
• February 10, 2025: Headache and Facial Pain and Neuro-diagnostics, 25 minutes
• February 17-21, 2025: First shifting examination
• February 24, 2025: Altered consciousness (Feb 25 EDSA) and Headache and facial pain, 20 minutes, Total 100 minutes
• March 3, 2025: Stroke and altered consciousness, 20 minutes
• March 10, 2025: Traumatic Brain Injury and Stroke, 30 minutes
• March 17, 2025: Traumatic Spinal Cord Injury and TBI, 20 minutes
• March 24, 2025: Second shifting examination
• March 31, 2025: Demyelinating Disease and TSCI, 30 minutes, Total 100 minutes
• April 7, 2025: Parkinson's disease (April 9 Araw ng Kagitingan) and Demye, 30 minutes
• April 14-21, 2025: Easter break
• April 21, 2025: MND and PD, 30 minutes
• April 28, 2025: Peripheral nerves and MND, 20 minutes
• May 5, 2025: NMJ and muscles and peripheral nerves, 20 minutes, Total 100 minutes

Sensorium Components

• Consciousness
• Attention span
• Orientation to time, place, and person
• Fund of information about surroundings
• Insight, judgement, and planning
• Calculation

Sensorium Functions

• Awareness of being aware
• Recognition of self and environmental awareness
• Registering internal and external contingencies
• Relates stimuli to memories, future hopes, and desires
• Attaching emotion and priority to incoming stimuli
• Proposes actions with consequences
• Directs motor system for survival and satisfaction
• Allows conscious experience of life, linking past, present and future

Sensorium Input and Adaptive Behavior

• Ascending pathways lead to the cerebrum
• Eyes, ears, nose, tongue, and skin through exteroceptors
• Vestibule, muscles, and tendons, via proprioceptors
• Thoracicoabdominal viscera via interoceptors
• Adaptive behavior results in survival and satisfactions

Consciousness Elements

• Arousal (Wakefulness): Integrity of the ascending reticular activating system (ARAS) which connects to the thalamus and is always active.
  • ARAS is made of neurons lying within the tegmentum in upper half of brainstem.
• Awareness (Content): Integrity of the cerebral cortex which dictates motor activity, as well as the quality and coherence of thought and behavior

Normal Alertness

• Individuals are responsive to thoughts or perceptions
• Indicates awareness of self and environment as that of the examiner
• Attention to, and interaction with immediate surroundings
• Alertness can fluctuate during the day

Confusion

• Inability to think with speed, clarity or coherence
• Impaired judgement and decision making
• Often due to encephalopathies or dementia affecting the whole brain
• Confused patients often have no memory of events
• Testing involves recall events
• Detecting defects in working memory involves: serial subtraction or spelling backwards or digit span and backwards, also impaired registration.

Confusion Characteristics

• Incorporation of clouded interpretation of internal and external experiences
• Inability to integrate and attach symbolic meaning to experiences (apperception)
• Degree of confusion varies hourly
• Least pronounced in the morning but increasing as the day wears on
• Confusion peaks in the early evening hours, which is known as "sundowning"
• This is common in dementia

Delirium

• Comes from the Latin term "to go out of the furrow"
• Characterized Severe inattentiveness, altered mental content and sometimes hyperactivity
• Stimuli are often misperceived, causing hallucinations
• Disorientation is first to time, then place, and lastly people in their environment

Delirium Tremens Symptoms

• Tremors in hands
• Chest pain
• tachycardia
• High blood pressure
• Fainting
• Confusion, anxiety
• Hallucinations
• Heavy sweating, pale skin
• Fever
• Nausea and vomiting
• Sleepiness or fatigue
• Sensitivity to light/sound
• Severe Dehydration
• Hyperactivity or excitability
• Seizures
• Often as result of alcohol withdrawal

Drowsiness

• Inability to sustain a wakeful state without external verbal stimuli application
• Inattentiveness and mild confusion that improves with arousal
• Decreased mental, speech, and physical activity
• Natural and unprompted shifting of positions
• Drooping eyelids, snoring, and relaxed limbs

Obtundation

• Comes from Latin term meaning "to beat against or blunt"
• Mental blunting
• Mild-to-moderate reduction in alertness
• Little interest in the surroundings
• Slow response to stimulation
• Responsiveness to non-painful physical stimulation

Stupor

• Defined as "to be stunned."
• It is a deeper state than drowsiness
• Patient can be roused only by vigorous, repeated painful stimuli
• Stimulation is required to sustain arousal
• Responses to spoken commands are absent, curtailed, or slow and inadequate
• Reduction or Elimination of shifting positions
• Eyes displaced slightly out and up, same as in sleep

Distinguishing Drowsiness from Stupor

• Drowsiness: responds to verbal stimulation or commands.
• Obtundation: responds to light, superficial, nonpainful stimulation
• Stupor: responds to noxious stimulation, such as trapezius squeeze, sternal rub, deep nail bed pressure, or supraorbital pressure.

Coma

• Comes from the Greek term meaning "deep sleep or trance"
• Incapable of arousal by external stimuli or inner need
• Lighter stage: Corneal, pupillary, and pharyngeal reflexes can be elicited.
• Deepest stage: No reaction of any kind can be obtained, corneal, pupillary, and pharyngeal responses are diminished.

Persistent Vegetative State

• Patients recover from coma and return to a state of wakefulness without cognition.
• Eyes-open permanent unconsciousness with loss of cognitive function and awareness of the environment but preservation of sleep-wake cycles and vegetative function.
• Vegetative syndrome of unconscious awakening for ≥3 months after nontraumatic brain injury or ≥12 months after traumatic injury = persistent
• The worst prognosis being anoxia from ischemia ex: MI
• Metabolic or encephalitic coma
• Head trauma

Signs of Vegetative State

• Severe cerebral injury leads to coma.
• Eyes open in response to pain, later spontaneously with increasing periods.
• Eyes may blink in response to threat or light
• Eye movement may follow stimulation or fixate
• Automatism like swallowing, grimacing, grunting, and moaning may occur
• Primitive postural and reflex movements Loss of sphincter control
• Respiration may quicken in response to stimulation
• A patient remains unresponsive for the most part; no speech, signs of awareness, or purposeful behavior.

Persistent Vegetative State Diagnosis

Laboratory Tests:

• EEG: Lack of normal change in background EEG activity during and immediately after stimulating patients
• Neuroimaging: Progressive and profound cerebral atrophy

Brain Death

• Coma where the brain was irreversibly damaged and has ceased functioning
• Pulmonary and cardiac function could still be maintained artificially
• State of complete unresponsiveness stimulation, arrest of respiration, and absence of EEG activity for 24 hours.
• Death can be called in the absence of cardiac function

Elements Determining Brain Death

• Absence of all cerebral functions
• Absence of all brainstem functions, including spontaneous respiration
• Irreversible state

Brain Death Characteristics

• Complete absence of cerebral function.
• Characterized by a deep coma, where all voluntary movement as well as motor responses to all auditory, visual and cutaneous are absent

How the Brainstem Functions in Brain Death

• Loss of pupillary response
• Loss of corneal, oculocephalic, and oculovestibular reflex, gag and cough reflexes
• Absence of facial movement to noxious stimuli
• Absence of cerebrally mediated movement to noxious stimulation of extremities

Brain Death Testing

Ensure injury history, exam and neuroimaging align with irreversible catastrophic injury

• Apnea test:
  • Destruction of the medulla
  • PaCO2 60mmHg (normal 35-45mmHg)
  • There is an unresponsiveness of medullary centers to high carbon dioxide tension in the blood
  • Absence of tachycardia in response to atropine indicates medullary vagal neurons damage

How the Apnea Test is Performed

• 1 Disconnect ventilator,
• 2 Catheter at carina, 100% O2 at 6L/min, observe chest and abdominal wall for movements, monitor vitals
• 3 Assess respiratory movements for 8 min, arterial blood gas, PCO2 reaches 60mm Hg or PCO2 increases over 20mm Hg

EEG in Brain Death Confirmation Electro Cerebral Silence

• Confirms cerebral death, indicating electrocerebral silence, shown in a flat or isoelectric EEG. Other confirmatory tests are digital subtraction angiography, the CTA, MRA, SPECT, and TCD. Other tests can rule out reversible causes like toxicology
• Hypothermia, Intoxication and sedative hypnotic drugs can cause reversible EEG with brainstem reflexes immediately after cardiac arrest

Glasgow Coma Scale (GCS)

• Developed in 1974 by University of Glasgow neurosurgery professors Graham Teasdale and Bryan Jennett
• It is used to objectively describe the extent of impaired consciousness in all types of acute medical and trauma patients.
• It is used to quickly communicate with other medical professionals

Parts of GCS

• Eye opening
• Verbal response
• Motor response

Glasgow Coma Scale (GCS) - Procedure

• Check for factors interfering with communication, injuries and ability to respond
• Observe eye-opening, content of speech, and movements of right and left sides to see if it's spontaneous.
• Stimulate with sound, such as a spoken or shouted request, or physically, with pressure on finger tip, trapezius or supraorbital notch
• Assign highest observed response

GCS Scoring

• Highest score: 15
• Lowest score: 3

GCS Eye Opening (E)

• 4 – opens eyes spontaneously
• 3 – opens eyes to voice
• 2 – opens eyes to pain
• 1 – no eye opening

GCS Best Verbal Response (V)

• 5 – appropriate and orientated
• 4 – confused
• 3 – inappropriate words
• 2 – incomprehensible (moans/groans/sounds)
• 1 – no sound
• NT – not testable (e.g., intubated)

GCS Best Motor Response (M)

• 6 – obeys commands
• 5 – localizes to pain
• 4 – withdraws to pain (normal flexion)
• 3 – abnormal flexor response
• 2 – abnormal extensor response
• 1 – no movement

Flexion Responses

• Abnormal Flexion (decorticate): Slow Stereotyped, Arm across the chest, Forearm rotates, Thumb clenched, Leg extends
• Normal flexion: Rapid, Variable, Arm away from body

Glasgow Coma Scale - Pupil

• GCS-P was developed in 2018 by Paul Brennan, Gordon Murray and Graham Teasdale
• GCS-P is a 4th number is (pupil reactivity score, PRS) that is subtracted from the standard GCS score and reflects the original score
• Formula: GCS-P = GCS – PRS
• Range of score from 1-15

Pupil Reaction GCS Score Table

• Score 2: Neither pupil reacts to light.
• Score 1: One pupil doesn't react to light.
• Score 0: Both pupils are reactive to light.

Head Injuries/Traumatic Brain Injury (TBI) & the Glasgow Coma Scale

• Mild TBI has a GCS scale score of 13-15
• Moderate TBI has a GCS scale score of 9-12
• Severe TBI has a GCS scale score of 3-8
• With GCS-P if score is 1-8 then it is considered severe

Initial Diagnostic Work Up and Emergent Management involves

• Establish and maintain airway, breathing and circulation
• Monitor vital signs
• Initial fluid management
• Assess neurologic function
• Laboratory screening
• Initiate specific treatment
• Obtain detailed history and perform systematic examination
• Perform additional diagnostic tests

What Makes a Case Neurologic?

• Focal Neurologic Deficit
• Increased ICP
• Meningeal Irritation

Categories of Neurologic Problems

• Congenital/developmental
• Trauma
• Infectious
• Degenerative
• Metabolic/endocrine
• Nutritional
• Vascular
• Demyelinating
• Immunologic
• Neoplastic

Neurologic Problem Categories

• Trauma: epidural/subdural/subarachnoid/intracerebral hemorrhage
• Infections: meningitis, encephalitis, brain abscess
• Diseases that are degenerative
• Mass lesion/neoplastic: neoplasm, abscess, hematoma, granuloma, cyst
• Vascular: cerebral infarction/hemorrhage/SAH
• Metabolic/endocrine
• Nutritional deficiency
• Immunologic
• Demyelinating

Temporal Profile of Disease

• Vascular issues are the most rapid
• Mass issues are the slowest

Types of Brain Lesions

• Focal: mass lesion, infarction, hematomas
• Multifocal: multiple tumors, mass lesions
• Diffuse: metabolic endocrine, toxic encephalopathy

Causes of Alteration in Consciousness

• Structural: refers to discrete lesions (ex. hematoma), widespread destructive changes of the hemispheres, and increased ICP
• Functional: refers to metabolic, toxic, nutritional d/t neuronal failure in the cerebrum and RAS

Discrete Lesions

• Secondary compression of the ARAS: Large mass in one cerebral hemisphere like tumor, abscess, massive infarct, etc. or large cerebellar lesion
• Destructive lesion immediately within thalamus or midbrain With ARAS still sending the signal but Cortex doesn't work

Widespread Bilateral Damage

• Widespread damage affects cortex and cerebral white matter like trauma, bilateral strokes or hemorrhages, encephalitis, meningitis, hypoxia, or global ischemia.
• This is defined as an interruption of thalamocortical impulses or generalized destruction of cortical neurons

Head Trauma

• Structural Lesions
• Can cause intracranial complications
• These being: epidural hemorrhage subdural hemorrhage, subarachnoid hemorrhage, intracerebral hemorrhage
• Head trauma is considered acute EXCEPT for subdural hematomas that can be acute, subacute, or chronic

Cerebrovascular Accident

• Structural lesion due to infarction or hemorrhage
• Acute
• Ischemic; clot in carotid extends directly into middle cerebral artery
• Hemorrhagic; subarachnoid hemorrhage from ruptured aneurysm, an example being from heart when clot fragments are transported

Types of Infection that affect the Brain

• Meningitis: a structural lesion, inflammation or swelling of the thin tissue-layer (meninges) surrounding the brain and spinal cord.
• Encephalitis: a diffuse lesion, inflammation of the brain itself
• Meningoencephalitis: Inflammation of both the meninges and the brain
• Maybe acute, subacute, or chronic
• Abscess: a focal/multifocal and chronic lesion
• Acute meningitis: (+) fever
• Subarachnoid hemorrhage: (-) fever
• Chronic meningitis: (+) fever

Case Study 1

• 22 year old who is male
• History: 4 days of fever, headache, body malaise and loss of appetite
• BP 100/70 Febrile 39.7C
• Pt is drowsy
• Arousable to name but remains sleepy, orientated to place, time and person, able to follow simple commands with a Glasgow Coma Scale (GCS) of 14 (E3V5 M6)
• Positive test: There is resistance on passive neck flexion

Case Study 1 Questions

• What is the level of consciousness of the patient?
• What is the GCS score of the patient?
• What is the GCS-P score of the patient?
• Resistance on passive neck flexion is nuchal rigidity.
• What makes the problem neurologic?
• What is the cause of the alteration in sensorium?

Meningeal Irritation and Fever

• Acute Meningitis: (+) fever
• Subarachnoid Hemorrhage (-) fever
• Chronic Meningitis (+) fever

Investigating Meningeal Irritation and Fever

• Investigate with a cranial CT scan
• CSF examination

Case Study 2

• 70 year old female
• Complaining of weakness of the left hand which is new
• History: 6 months of progressively increasing severity and frequency of frontotemporal headache and change in pattern
• BP 130/70 PR 70 afebrile

Neurological Examination

• Spontaneous eye opening, appropriate responses to questions, follows commands
• Papilledema (both eyes)
• Motor score (MMT): 4/5 on the left upper and lower extremities
• Sensory score (deficit on the left side) _ Left Babinski sign

Case Study 2 Questions

• What is the level of consciousness of the patient? normal
• What is the GCS score of the patient? 16, E4B5
• What is the GCS-P score of the patient? 15
• What makes the problem neurologic? Papilledema

Focal Neurologic Deficits based on Cerebrum

• Disturbance in higher intellectual functions
• Seizure
• Language problem
• Behavioral, personality and mental changes
• Contralateral hemiparesis with Babinski
• Contralateral hemisensory deficit
• Visual field deficit

Focal Neurologic Deficits based on Brain Stem

• CROSSED MOTOR/SENSORY SYNDROME:
• Ipsilateral cranial nerve deficit
• Contralateral hemiplegia with Babinski
• Contralateral hemisensory deficit

Focal Neurologic Deficits based on Cerebellum

• Truncal ataxia
• Limb ataxia

Differential Diagnoses for Focal Brain Dysfunctions

• Can be acute or chronic
• Acute: Vascular from ischemic or hemorrhagic stroke
• Chronic: Degenerative or there is a mass lesion such as Neoplastic, Abscess, Hematoma, Granuloma, Cyst

Increased Intracranial Pressure Symptoms

• Increased Intracranial Pressure is the result of pseudotumor cerebri

Increased Intracranial Pressure Causes

• Can be acute stemming from : Trauma (resulting in Epidural Hematoma, Subdural Hematoma, Subarachnoid Hemorrhage, Parenchymal Hemorrhage), fever resulting in Acute Meningitis, and a stroke resulting in Cerebral Infarction or SAH
• Can be chronic: Mass Lesion (Tumor), Chronic Meningitis, Hydrocephalus

How to Investigate for Increased Intracranial Pressure

• Anillary testing: Cranial CT scan, Cranial MRI
• Negative cranial imaging: CSF examination, and it could be Pseudotumor cerebri

Altered Consciousness - Structural Lesions

• Structural Lesion causes MI, Increased ICP, FND which can be investigated with cranial imaging or CSF examination as well as checking for hemorrhagic complications of trauma, CVA, mass lesion, meningitis

The metabolic causes for alteration of consciousness

• 1, Glucose levels (increased or decreased)
• 2. Oxygen levels (diminished)
• 3. Fluid volume (increased or decreased)
• 4. Electrolytes (increased or decreased)
• 5. Acidosis or alkalosis
• 6. Excess endogenous waste (creatinine, ammonia, CO2)
• Toxic causes: Exogenous toxins, poisons, chemicals, drugs
• Nutritional deficiency: b 1, b6, b12

Causes of Altered Consciousness due to Encephalopathy

• Behavioral and personality changes may be the initial presentation
• Acute confusional episode or Delirium
• Alteration of consciousness
• Generalized seizures
• Functional Neurological Disorder’s are usually absent but if present, they are bilateral Babinski

Altered Consciousness - Functional Lesions

• Functional Lesion can cause MI, Increased ICP, FND
• This can cause an Encephalopathy
• Which results in Metabolic-endocrine, Toxic, Nutritional deficiency (B1,B6, B12)

Lesions Causing Loss of Consciousness

• Primary brainstem lesion
• Bihemispheral lesion: herniation syndromes
• Secondary brainstem compression
• Encephalopathy (toxic, metabolic, hypoxic)