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Neuroscience > Module 8 > Flashcards

Module 8 Flashcards

1
Q
  • Not just medical, but literary, philosophic and psychologic
  • The state of the patient’s awareness of self and environment and his responsiveness to external stimulation and inner need
  • it is operational; you have to do something to detemine it.
A

consciousness

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2
Q

how to know if the patient is conscious?

A
  1. observe the patient

2. talk to the patient and see if he/she is responsive

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3
Q

2 components/ dimensions of consciousness

A
  1. content/cognition - what the patient knows

2. arousal - level of wakefulness; may be elevated or depressed

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4
Q

Elevation of Arousal

A
  • Insomnia
  • Euphoria
  • Mania
  • Hallucinations
  • Convulsions
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5
Q

Depression (Level of Arousal)

A
  • Normal Sleep
  • Somnolence
  • Stupor
  • Semicoma
  • Complete Coma
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6
Q

States of Normal and Impaired Consciousness

A
  1. Normal Consciousness
  2. Confusion
  3. Drowsiness/ Somnolence - patient drifts to sleep but easily be aroused by light tapping or name calling
  4. Stupor - patient drifting to sleep but can only be aroused by vigorous tapping; patient should respond after stimulating
  5. Coma – light (semicoma) or deep coma
    Deep coma- absence or brain reflex
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7
Q

Structures necessary for consciousness

A
  1. Rostral pontine tegmentum
  2. Midbrain tegmentum
  3. Diencephalon
  4. Caudate-putamen (striatum)
  5. Medial hemispheric wall
  6. One cerebral hemisphere (esp. the cortex) and corresponding deep white matter
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8
Q

What is in the tegmentum that is necessary for the wakefulness?

A
  • In the Tegmentum, you see The Ascending Reticular Activating System (RAS)
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9
Q

What is in The Ascending Reticular Activating System (RAS)?

A
  • loosely organized group of neurons; no distinct borders; seen in the tegmentum
  • consists of neurons that uses different neurotransmitters (cholinergic, histaminic, serotonergic) that are part of the reticular activating system
  • they send projection to the thalamus as well as cingulate gyrus and diffusely to other parts of the cerebral hemisphere.
  • also accepts information from the sensory pathway (from spinothalamic tract and tigeminothalamic tracts)
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10
Q

Reticular Activating System (RAS) stimulation and disruption

A

Stimulation: transient arousal
Disruption: depression of consciousness/coma

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11
Q

Metabolic Mechanisms that Disturb Consciousness (1)

A
  • Reduction in blood flow (eg shock, low BP, arrest)
  • Reduction in cerebral metabolism (hypoglyceima)
  • Toxins – endogenous toxins (hepatic encephalopathy - hyperammonemia; kidney problems - increase creatinine); hypoNatremia (blood will be hypotonic causing shifting of fluids inside the neuron that will cause swelling); direct effect on neuronal membranes in the cerebrum, RAS, neurotransmitters and their receptors
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12
Q

Metabolic Mechanisms that Disturb Consciousness (2)

A
  • Sudden and excessive neuronal discharges – as that which occur in seizures (particularly generalized seizures)
  • Concussion - brought about by tremendous pressure; shearing forces from trauma/accident; can be temporary
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13
Q

Pathologic Anatomy of Coma (Structural Causes of Coma)

A
  1. Discernible mass lesions (if the mass is large, it can cause increase pressure in the brain leading to brain herniation)
  2. Destructive lesions in the midbrain or thalamus
  3. Widespread bilateral damage to the cortex, cerebral white matter
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14
Q
  • a displacement/dislocation of brain tissue from one compartment to another
  • name based on the structure that is traversed or part that is herniating
A

Herniation

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15
Q

Schematic Depiction of brain herniations (Cerebral hemispheric subcortical white matter)

A
  1. Transfalcine or subfalcinar lesion - herniation under the falx cerebri
  2. Transtentorial Herniation or Uncal Herniation - downward displacement and it passes through the tentorium cerebelli
  3. Cerebellar Tonsillar Herniation/Transforaminal Herniation - passage of the cerebral tissue to the foramen magnum
  4. Kernohan-Woltman Notch/Phenomenon - not a herniation but occurs in uncal herniation
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16
Q

Types of Transtentorial Herniation

A
  1. Uncal Herniation Syndrome - medial portion of the temporal lobe herniate
  2. Central Herniation Syndrome - entire brain that is displaced downward so there is lateral involvment
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17
Q
  • follows a rostro-caudal sequence (confusion, apathy, drowsiness) then sensorial change
  • may notice Cheyne-stokes respiration
  • pupils are small which reach sluggishly to light&raquo_space; bilateral decerebration&raquo_space; loss of caloric responses&raquo_space; irregular breathing&raquo_space; death
A

Central Syndrome

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18
Q

• Preceded by a unilateral pupillary dilatation (because of impingement of Cranial Nerve III which emeges from the midbrain; malapit na sa tentorium cerebelli kaya pagnaherniate na ang uncus, madali syang maimpinge)

A

Uncal Syndrome

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19
Q

Pathologic Changes in uncal herniation:

A
  1. Injury to outer fibers of ipsilateral CN III
  2. Creasing of contralateral cerebral peduncle (Kernohan’s notch)
  3. Duret hemorrhages
  4. Unilateral or bilateral infarction of the occipital lobes - there might be impingement of the arteries (posterior cerebral artery causing secondary strokes)
  5. Rising ICP and hydrocephalus (accumulation of CSF due to obstruction in the aqueduct of sylvius; hydrocephalus will be more seen in the lateral ventricle)
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20
Q

Clinical Manifestation of the Creasing Contralateral Cerbral Peduncle (Kernohan Notch)

A

Crushing of the cerebral peduncle which contains the corticospinal fibers (Contralateral to kernohan’s notch weakness and extensor problem

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21
Q
  • small hemorrhages in the midbrain brought about by small torn arteries
A

Duret hemorrhage

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22
Q
  • Impaired consciousness
  • Neck rigidity
  • Opisthotonus and decerebrate rigidity
  • Irregular respiration
  • Apnea that can lead to respiratory arrest
  • Bradycardia
A

Cerebellar tonsillar herniation

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23
Q

Posturing (reason of rostrocaudal sequence in Central Herniation)

A
  1. Supratentorial Lesion - weakness contralaterally
  2. Upper midbrain damage - decorticate posturing (abduction of the upper extremity, flexion of the wrist, stiffening of bilateral lower extremities)
  3. Upper pontine damage - decerebrate (extended Upper extremities and externally rotated, Lower extremities stiffened
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24
Q

Respiratory and autonomic effects of brainstem lesions and transtentorial herniation

A
  1. Supratentorial lesion - apnea then increase respiration then apnea (Cheyne-Stoke respiration: earliest sign that you’ll know that there’s something happening in the brain but not all the time neurologic)
  2. Upper midbrain lesion - rapid inspiration and expiration (Central Neurogenic Hyperventilation; can be seen also in acidotic patients and pneumonia)
  3. Pons lesion - inspiration, pause, apnea (Apneustic Breathing; not a good type of respiratory breathing)
  4. Caudal Pons lesion - irregular, no characteristics - can be shallow, deep then periods of apnea (Ataxic Breathing/ Biot breathing/agonal type of respiration); usually poor prognosis
  5. Medulla - apnea (no breathing)
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25
Q

Pupils of the Unconscious patients (can have a clue on the cause of the trauma)

A
  1. Metabolic Disturbances - reactive and equal
  2. Diencephalic Lesion - small, equal and reactive
  3. Uncal herniation - one pupil will be dilated (usually the one ipsilateral to the herniation)
  4. Midbrain lesion - midposition pupils (not too large, not too small) and usually fixed
  5. Pontine lesion - pinpoint pupil (usually you cannot discern the reaction of the pupil because it is too small)
  6. Pretectal lesion - large, fixed, hippus
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26
Q

Approach to a Patient with Impaired Consciousness (Initial assessment)

A 
I. Initial assessment:
• Vital signs – pressors?
• Airway – be prepared for intubation
• Blood sugar – glucose with thiamine
• Assume a possible cervical spine injury until it is ruled out
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27
Q

Approach to a Patient with Impaired Consciousness (History)

A

II. History:
• Sequence of events leading to coma
• Patient’s past medical history and medications – check also for suicidal attempts

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28
Q

Approach to a Patient with Impaired Consciousness (Physical Examination)

A

III. Physical Examination
• Vital signs – especially respiration, heart rate
• Signs of trauma? any wounds
• Signs of acute or chronic illness
• Neurologic examination: level of consciousness, pupils, eye movements, fundoscopy, motor status, reflexes, meningeal signs

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29
Q

How can you elicit pain in a patient having decreased in sensorium?

A

a. Pressure on the supraorbital nerve - apply pain on the orbital rim
b. Pressure on the nail bed
c. Sternal rub

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30
Q
  • scale that was developed on patients who had trauma
  • way of assessing the level of brain injury
  • consists of 3 parts: Eye opening, Best Verbal response and Best Motor Response
A

Glasgow Coma Scale

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31
Q

Eye Opening

A

4 – Spontaneous
3 – To speech
2 – To pain
1 – None

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32
Q

Best Verbal Response

A 
5 – Oriented
4 – Confused
3 – Inappropriate
2 – Incomprehensible
1 – None
(if pt in intubated, don't put a score, just put T/intubated)
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33
Q

Best Motor Response

A

6 – Obeying/ follows commands
5 – Localizing (will tell you where is the pain; withdraw on where the pain is)
4 – Withdrawal (cannot localize but can withdraw, flexion of the arm, parang hilaw na localization na pain)
3 – Flexion (decorticate)
2 – Extension (decerebrate)
1 – None

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34
Q

What if the patient is aphasic but can do spontaneous movements? What can you grade on the Best motor response?

A

6

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35
Q

Glasgow Coma Score

A

Normal - 15

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36
Q

(Differentiating coma due to metabolic vs. structural disorders)
Focal/Lateralizing Sign

A

Structural

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37
Q

(Differentiating coma due to metabolic vs. structural disorders)
Pupil reactivity

A

Metabolic - reactive pupil and equal although not always but its a general rule

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38
Q

(Differentiating coma due to metabolic vs. structural disorders)
Eye movements

A

Structural - doll’s eye but if its in the brainstem there will be no doll’s eyes

Metabolic - intact doll’s eye

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39
Q

Brain Death: Primary Clinical Criteria

A
  • …has suffered a condition that could cause brain death
  • …receiving artificial respiration
  • …minimum core body temp of 32.2°C (mature)
  • …normotensive (coma state is not due to circulation
  • …no depressants/ neuroparalytics administered to the patient
  • …no brainstem functions
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40
Q

What is “no brain functions”?

A
  1. coma
  2. midposition/ dilated pupils
  3. no spontaneous/ induced eye movements
  4. no response to Vth nerve stimulation (no corneal reflex)
  5. no spontaneous or reflex facial movements
  6. no oropharyngeal responses
  7. no audito-palpebral or vestibulo-ocular reflexes (doll’ eye reflex) - (introduce a loud sound and if the patient didn’t blink it will be a negative audito-palpebral reflex)
  8. complete apnea
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41
Q

Ancillary Diagnostic Tests for Brain Death

A
  1. Isoelectric EEG – “electrocerebral silence” (similar to flatline on EKG)
  2. Absence of cerebral blood flow by radionuclide or Doppler studies or direct angiography
  3. Apnea test - oxygenate the pt for sometime and if you remove it pt will demonstrate increasing carbon dioxide level); pt who doesn’t breath will not be able to blow off CO2
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42
Q

Etiologies of Coma: Metabolic and other diffuse disorders

A
  • Drug poisoning
  • Anoxia or ischemia
  • Hepatic encephalopathy
  • Encephalomyelitis and encephalitis (infection of the brain)
  • Subarachnoid hemorrhage (bleeding on the subarachnoid space usually by bleeding or trauma)
  • Endocrine disorders (e.g., diabetes) - hypoglycemia
  • Acid-base disorders - renal diseases
  • Temperature regulation - hypothermia
  • Uremic encephalopathy
  • Pulmonary disease
  • Nutritional
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43
Q

Etiologies of Coma: Supratentorial mass lesions

A
  • Intracerebral hematoma
  • Subdural hematoma
  • Cerebral infarct
  • Brain tumor
  • Epidural hematoma
  • Thalamic infarct
  • Pituitary apoplexy
  • Closed head injury
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44
Q

Etiologies of Coma: Infratentorial lesions

A
  • Brainstem infarct
  • Pontine hemorrhage
  • Cerebellar hemorrhage
  • Cerebellar infarct
  • Brainstem demyelination
  • Cerebellar abscess
  • Posterior fossa subdural hemorrhage
  • Basilar migraine
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45
Q
  • …exhibit sleep-wake cycles
  • …appear awake
  • …responds to pain but not purposive
  • …akinetic or hypokinetic
  • …may retain autonomic or somatic reflexes
  • …may show primitive reflexes
A

Persistent vegetative state (PVS)

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46
Q
  • …the patient is capable of some rudimentary behavior, or producing simple words and phrases
  • …difficult to differentiate from akinetic mutism
  • …often exists as a transitional state arising during recovery from trauma or worsening of progressive neurologic disease
A

Minimally Conscious State

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47
Q
  • Affectation of the basis pontis, leaving the pontine tegmentum intact
  • Patient is conscious, quadriplegic and can move eyes vertically
A

Locked-In Syndrome

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48
Q
  • …coma vigile
  • …intact motor and sensory pathways
  • …profoundly abulic and apathetic
A

Akinetic Mutism

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49
Q
  • Catatonia
  • Reflexes are preserved
  • Waxy flexibility (maintaining a posture), catalepsy
A

Psychogenic Unresponsiveness (Hysterical Coma)

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50
Q

Outline of Mental Status Examination

A
  1. General behavior and appearance
  2. Stream of talk
  3. Mood and affective responses
  4. Content of thought
  5. Intellectual capacity - pt education
  6. Sensorium
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51
Q

Sensorium

A
  1. Consciousness (awake, drowsy)
  2. Attention Span - ability of the pt to focus; give attention to a specific topic
  3. Orientation for time, place and person -
  4. Memory, recent and remote
  5. Fund of information - pt education, current events
  6. Insight, judgment and planning
  7. Calculation
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52
Q
  • term usually used to refer to the gnosias (to know)

* Certain functions are assignable to certain cortical regions, i.e., motor and sensory activities

A

Higher Cortical Functions

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53
Q

True or False

Higher-order physiologic and psychologic function do not have a precise and predictable anatomy

A

True

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54
Q
  • Certain cerebral functions are the product of complex, diffusely distributed activity
  • …by which sensory stimuli are analyzed and integrated at various levels of the nervous system
  • …and are united through a system of temporarily acquired (experientially derived) connections, into a working mosaic adapted to accomplish a particular task.
A

Higher Cortical Functions

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55
Q

Higher Cortical Functions:

A
  • Cortex (gray matter) – 4,000 cm2 (roughly the size of the broad sheet)
  • 10-30 billion neurons
  • 150 billion glial cells (supporting cells)
  • Trillions of synaptic connections
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56
Q

Homotypical cortex vs Heterotypical cortex

A

Homotypical cortex – laminations are distinct; either granular or agranular

Heterotypical cortex – less discrete lamination

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57
Q
  • anterior to the frontal sulcus
  • precentral gyrus (motor cortex, Brodmann Area 4)- gyrus that is anterior to it
  • Anterior to the precentral lobe is divided by 3 sulci into 3 gyri: superior, middle, inferior
  • inferior gyrus contains pars orbitalis, pars triangularis (BA 44/45 Broca’s Area) and pars opercularis
A

Frontal lobe

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58
Q

Brodmann Area in the Frontal Lobe

A

BA 6 - Premotor
BA 8 - ocular motility
BA 9-12 - Prefrontal lobe
BA 45-47 - responsible for behavior and spontaneity of response

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59
Q

Clinical Effects of Frontal Lobe Lesions (1)

A
  1. Motor abnormalities – motor cortex
  2. Speech and Language disorders – related to the dominant hemisphere (can result to Broca’s aphasia)
  3. Incontinence of bowel and bladder - area of frontal lobe that is for urination; found in the medial portion; usually kung saan saan na lang umiihi
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60
Q

Clinical Effects of Frontal Lobe Lesions (2)

A
  1. Impairment of attention, concentration, capacity for sustained mental activity, ability to shift from one line of thought or action to another
  2. Akinesia, apathy and abulia (matagal magresponse); utilization behavior (if you present an object, there is a desire to manipulate that object)
  3. Disinhibition of behaviour (perseveration -hindi makaalis from a previous thought)
  4. Distinctive abnormality of gait (gait apraxia - no weakness on the legs but have ataxia, also called as magnetic gait because it seems to be stuck to the ground and shuffling)
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61
Q

Neurologic Examination Techniques (Frontal Lobe)

A
  1. Observation during history taking

2. MMSE, MOCA (Montreal Cognitive Assessment)– with some components of frontal assessment

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62
Q
  • primitive reflexes that are seen in babies and have disappeared because the frontal lobe stimulates them from appearing
  • Grasp Reflex, Rooting reflex (stroking the side of the lips can cause the patient to go towards the stimuli), Palmomental reflex (stroking of the thenar eminence of one hand will cause contraction of the muscle ipsilateral to the hand), Sucking Reflex, Glabellar Tapping
A

Frontal Release signs

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63
Q
  • repeated blinking if you tap on the glabella

- Normal: can have few blinks but eventually pt will resist blinking

A

Glabellar Tapping

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64
Q
  • inferior to the Sylvian Fissure
  • divided by 2 sulci into superior, middle and inferior gyrus
  • superior gyrus - primary auditory cortex (Brodmann area 41/42)
  • anterior to the primary auditory cortex is Brodmann area 22 (association area)
  • inferior part for association words and vision
  • amygdala and hippocampal formation are found here (middle portion)
A

Temporal Lobe

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65
Q

Clinical Effects of Temporal Lobe Lesions (1)

A
  1. Visual Disorders - because part of the optic radiation pass through the temporal lobe particularly those subserving the upper fields
    Field cuts - superior quadrantanopsia
    Visual hallucinations
  2. Cortical deafness
  3. Auditory agnosias
    Agnosia for sounds - can hear but cannot identify the sounds
    Amusia - agnosia for music
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66
Q

Clinical Effects of Temporal Lobe Lesions (2)

A
  1. Word deafness (Auditory verbal agnosia) – the essential element in Wernicke’s aphasia; hear spoken words but you cannot process it
  2. Auditory illusions
  3. Auditory hallucinations
  4. Vestibular disturbances
  5. Disturbances of time perception
  6. Disturbances of smell and taste
  7. Disorders of memory, emotion and behavior
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67
Q

Broca’s Aphasia vs Wernicke’s Aphasia

A

Broca’s Aphasia - comprehension is intact but the speech is not fluent, repetition is poor

Wernicke’s Aphasia - Comprehension is poor but speech is fluent; speech is also incoherent

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68
Q

Neurologic Examination Techniques

A
  1. Confrontation test

2. Halstead-Reitan-Wepman screening test (as described in De Myer)

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69
Q
  • posterior to the post central gyrus (BA 3,1,2 Primary Sensory Cortex)
  • Posterior to the post central gyrus is divided into 2 by the intraparietal sulcus: superior parietal lobule (above) and inferior parietal lobule (below)
  • Superior Parietal lobule contains BA 5 and 7 which is the association areas for sensation
  • Inferior Parietal lobule made up of 2 gyri (superior marginal gyrus and angular gyrus)
A

Parietal Lobe

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70
Q

Clinical Effects of Parietal Lobe Lesions (1)

A
  1. Cortical sensory syndromes
    • Position sense - proprioception
    • Astereognosis - ability to identify object based on shape
    • Agraphesthesia - ability to identify numbers/letters on the palm
    • Two-point discrimination - ability to discern whether it is one or 2
    • Detection of direction of movement of a tactile stimulus - directional scratch test
    • Tactile inattention or extinction - ability to attend to 2 sensory stimulus presented simultaneously
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71
Q

Clinical Effects of Parietal Lobe Lesions (2)

A
  1. Asomatognosias - inability to identify parts of the body
    • Anosognosia (hemispatial neglect) – may be manifested with:
    - Dressing apraxia
    - Constructional apraxia
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72
Q

– inferior parietal lobe problem; bilateral asomatognosia; consists of finger agnosia (unable to identify fingers), right-left confusion, dyscalculia, dysgraphia (inability to write)

A

Gerstmann Syndrome

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73
Q

Clinical Effects of Parietal Lobe Lesions (3)

A
  1. Ideomotor and Ideational Apraxia – loss of the ability to perform learned motor skills; usually affected the dominant parietal lobe
  2. Visual disorders - inferior quadrantanopsia (due to optic radiation passing through the parietal lobe)
    • Visual neglect (usually a part of hemispatial neglect)
    • Visual disorientation and topographognosia
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74
Q

Neurologic Examination Techniques (Parietal Lobe)

A
  1. Tactile inattention or extinction - inability to attend to 2 simultaneous stimuli; have to administer 2 stimuli at the same time
  2. Hemineglect – line bisection test; clock-drawing test; pt is presented with a line and pt has to put where the center of the line is
  3. Finger agnosia - inability to name finger; touch one finger at a time and identify the finger; ask pt show which finger was touched
  4. Right-left confusion - eg use your left hand to touch you right nostril
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75
Q

Neurologic Examination Techniques (Parietal Lobe) 2

A
  1. Dysgraphia
  2. Dyscalculia
  3. Tests for apraxia – may be done by giving various commands
  4. Dressing apraxia
  5. Tests for constructional apraxia - intersecting pentagon
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76
Q
  • no particular landmark just he parieto-occipital fissure

* contains the primary and association areas for vision

A

Occipital Lobe

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77
Q

Clinical Effects of Occipital Lobe Lesions

A
  1. Visual field defects - hemianopsia
  2. Cortical blindness
  3. Visual anosognosia
  4. Visual illusions and hallucinations
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78
Q

Clinical Effects of Occipital Lobe Lesions 2

A
  1. Visual agnosias
    • Visual object agnosia - pt can see but cannot identify
  • Simultanagnosia/ simultagnosia - has inattention on 2 simultaneous visual stimuli
  • Prosopagnosia - ability to identify familiar faces
  • Color agnosia - can see the color and can match on the other objects that have the same color but pt cannot identify the color
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79
Q

Neurologic Examination Techniques (Occipital Lobe)

A
  1. Visual agnosia – differentiate from anomia
  2. Prosopagnosia – show familiar, popular faces
  3. Simultanagnosia – bilateral visual stimuli
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80
Q

visual agnosia vs anomia

A

Visual agnosia - unable to identify the object

Anomia - cannot identify but knows the function of the object (hindi lang alam ang pangalan)

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81
Q

3 Primary Vesicles

A
  1. Prosencephalon/ Forebrain
  2. Mesencephalon/ Midbrain
  3. Rhombencephalon/ Hindbrain
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82
Q
  • will divide into Telencephalon and Diencephalon
  • Telencephalon: Cerebral cortex (two hemispheres), portions of basal ganglia
  • Diencephalon: Thalamus, hypothalamus, subthalamus and epithalamus
A

Prosencephalon

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83
Q
  • will be the same mesencephalon
A

Mesencephalon

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84
Q
  • will be divided into Metencephalon and Myelencephalon
  • Metencephalon: Pons and cerebellum
  • Myelencephalon: Medulla oblongata
A

Rhombencephalon

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85
Q

The __ is the region of the embryonic vertebrate neural tube that gives rise to posterior forebrain structures including the thalamus, hypothalamus, posterior portion of the pituitary gland and pineal gland.

A

diencephalon

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86
Q

Subdivisions of the Diencephalon:

A
  • Hypothalamus
  • Thalamus
  • Epithalamus
  • Subthalamus
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87
Q

• Extremely important in maintaining homeostasis. It does so by regulating 3 interrelated functions
1. Endocrine secretions – control hormones secreted by the pituitary gland
2. Autonomic Functions – integrates autonomic functions via direct projections to preganglionic autonomic neurons located in the brain stem
and spinal cord
3. Emotions and Drives – numerous interconnections with the limbic system

A

Hypothalamus

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88
Q

Hypothalamus: Supra-optic region

A

• Supraoptic nucleus – contains neurons that produce the ADH or vasopressin
• Paraventricular nucleus – produce oxytocin
• Suprachaismatic nucleus – involved in controlling circadian rhythms
• Medial Preoptic - Blood pressure
• Anterior Hypothalamic - Body
temperature

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89
Q

(Hypothalamus)

• Contain cells that produce orexins, which control the various aspects of sleep.

A

Tuberal region

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90
Q

(Hypothalamus)

• Mamillary bodies play a role in memory and learning

A

Mamillary region

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91
Q

Hypothalamus: Inputs

A
  • Nucleus of Solitary Tract – collects all of the visceral sensory information from the vagus
  • Limbic system – via the fornix. Help regulate behaviors like eating and reproduction
  • Retina – via direct branches of the optic nerve going to the suprachiasmatic nucleus
  • Blood – intrinsic receptors (thermoreceptor, osmoreceptors, chemoreceptors)
92
Q

Hypothalamus: Ouput

A
  • Neural signals to the autonomic nervous system via projections to the brain stem vagal nuclei and the the preganglionic nuclei in the spinal cord
  • Neural signal to the limbic system
  • Endocrine signal through the pituitary gland
93
Q
  • This gland is a very odd, and very important gland. Only half of this gland is diencephalic.
  • The neural part, the neurohypophysis
  • The glandular part, the adenohypophysis, derived from oral epithelium
A

Pituitary Gland

94
Q

(Pituitary Gland)

• Hypothalamus control endocrine system via:

A
  1. Direct secretion of neuroendocrine products
    into the general circulation via the vasculature of the posterior pituitary
  2. Indirectly by secreting releasing factors for the anterior pituitary
95
Q

• This may be seen with any disease within or near the pituitary gland and stalk that interferes with the delivery of dopamine (a neurotransmitter) from the hypothalamus to the prolactin secreting cells of the pituitary. Therefore, other types of pituitary adenomas, craniopharyngiomas or other tumors or masses may cause modest elevations in prolactin.

A

“stalk effect”

96
Q

• This large region is a relay station
• Main type of information that gets relayed here is sensory information. Motor is likewise
relayed.
• All sensory information going to the brain (except for olfactory) has to make a pit stop at the thalamus in order to be relayed appropriately

A

Thalamus

97
Q 
• Internal medullary lamina – runs longitudinally and separates the thalamus into medial and lateral nuclear masses
• 5 nuclear groups
- Medial
- Lateral
- Ventral
- Anterior
- Intralaminar
A

Thalamus

98
Q

• Nuclei: No important named nuclei
• Receives Input from: Limbic system (including
mammillary bodies)
• Cortical connections: Cingulate gyrus

A

Anterior

99
Q

• Nuclei: Mediodorsal Nucleus
• Receives input from: Olfactrory cortex and
spinothalamic
• Cortical Connections: Pain relayed to prefrontal.
- Olfactory relayed to insula and orbitofrontal cortex

A

Medial

100
Q

(Lateral)
• Nuclei: __
• Receives input from: Limbic System
• Cortical Connections: Cingulate gyrus

A

Lateral Dorsal

101
Q

(Lateral)
• Nuclei: __
• Receives input from: Different Sources
• Cortical Connections: Parietal, temporal, Occipital association cortex

A

Pulvinar and Lateral Posterior

102
Q

(Ventral)
• Nuclei: __
• Receives input from: Cerebellum, Globus
Pallidus, SNpr (substantia nigra pars reticulata)
• Cortical Connections: Motor and Pre-motor

A

Ventral Lateral and Ventral Anterior

103
Q

(Ventral)
• Nuclei: __
• Receives input from: Medial Lemniscus
• Cortical Connections: Somatic sensory

A

Ventral Posterior: Ventral Posterolateral/Ventral Posteromedial

104
Q

(Ventral)
• Nuclei: __
• Receives input from: inferior colliculus
• Cortical Connections: auditory cortex

A

Medial geniculate body (MGB)

105
Q

(Ventral)
• Nuclei: __
• Receives input from: Retinal Ganglion Cells
• Cortical Connections: Primary Visual Cortex

A

Lateral Geniculate body (LGB)

106
Q

(Intralaminar)
• Nuclei: __
• Receives input from: Ascending reticular activating system (ARAS), spinothalamic
• Cortical Connections: Diffuse

A

Sheet like

107
Q

(Intralaminar)
• Nuclei: __
• Receives input from: Glob. Palm SNpr (substantia nigra pars reticulata)
• Cortical Connections: Motor Cortex

A

Centromedian

108
Q

• If damage includes __ a contralateral hemianesthesia usually results. Typically ALL somatic sensory modalities are affected.

A

Ventral Posterolateral and Ventral Posteromedial

109
Q

• are sometimes seen after a period of recovery from damage to Ventral Posterolateral and Ventral Posteromedial. Such pain can be severe and intractable. These do not occur with lesions confined to the cerebral hemisphere

A

Hyperalgesia and spontaneous pain

110
Q

• IF Lateral Geniculate body (LGB) is affected there is a __

A

contralateral homonymous hemianopsia

111
Q

• If damage extend into the __, complex movement disorders can result. It is usually contralateral hemiplegia. Both the cerebellum and basal ganglia project to __

A

Ventral Lateral and Ventral Anterior

112
Q

• IF Medial Geniculate body (LGB) is affected there is a __

A

bilateral hearing loss

113
Q
  • Ventral to the thalamus and lateral to the hypothalamus
  • Plays a role in the generation of rhythmic movements
  • Stimulation of the STN (involves in involuntary movements) provides the most effective treatment for late stage Parkinson’s disease
A

Subthalamus

114
Q 
• Smallest and oldest part of diencephalon
• Composed of the:
- Pineal Body
- Habenula
- Posterior communicating Commisure
A

Epithalamus

115
Q

Epithalamus: Function

A
  • Linked to the limbic system
  • Autonomic
  • Endocrine
  • Reproductive (mating behaviour)
  • Circadian rhythm
116
Q
  • Synchronize or reset the circadian rhythm
  • It is a small midline mass of glandular tissue that secretes the hormone melatonin.
  • In lower mammals, melatonin plats a central role in control of diurnal rhythms
  • In humans, a portion of the control of diurnal rhythms has been taken over by the hypothalamus.
A

Pineal Gland

117
Q
  • It is a pair of small nuclei located above the thalamus at its posterior end.
  • It sits just in front of the pineal body.
  • Extending anteriorly from the habenula is the STRIA MEDULLARIS which is visible at the dorsal surface of the thalamus connecting to the limbic system
  • is divided into medial and lateral habenula, each has different functions
  • has projections to the limbic system
A

Habenula

118
Q

Habenula: Functions

A
  • Lateral habenula is associated with negative emotions. It is excited by nociceptive stimulus.
  • Habenular lesions disrupt female sexual behaviour and maternal behavior
  • Habenula is involved in the expression of circadian rhythm originating from the suprachiasmatic nucleus.
119
Q

Ear is subdivided in to three

A
  1. External Ear
  2. Middle Ear
  3. Inner Ear
120
Q

• External auditory meatus is formed by auricular and annular cartilages

A

External Ear

121
Q

• Three ossicles:
- malleus, incus, and stapes
- transmit tympanic membrane movements to
the membrane of the oval window

A

Middle Ear

122
Q

Two muscles reflexly dampen ossicle movement, to suppress forceful low frequencies:

A
  1. stapedius muscle, innervated by facial nerve (CN VII), pulls the stapes away from oval window;
  2. tensor tympani muscle, innervated by trigeminal nerve (CN V), pulls malleus thus tensing the tympanic membrane
123
Q

Middle Ear: Four openings (three sealed by membranes)

A 
1. Eustachian tube connects middle ear
to the nasopharynx;
2. tympanic membrane (ear drum) separates tympanic cavity from external auditory meatus;
3. oval (vestibular) window separates the tympanic cavity from perilymph in the
vestibule;
4. round (cochlear) window separates
tympanic cavity from perilymph in the
scala tympani;
124
Q

• consists of the cochlea and vestibular apparatus.
• The cochlea is a component of osseous labyrinth that contains perilymph and the cochlear duct
• The cochlear duct is a component of membranous labyrinth and contains endolymph.
• The cochlea makes 2.5 turns in man, around a core of bone (called the modiolus) through
which the cochlear nerve passes.

A

Inner Ear

125
Q

Within the cochlea, the cochlea duct (scala media) separates two perilymph chambers: the scala vestibuli, which contacts the oval window membrane, and the scala tympani, which contacts the __.

A

round window membrane

126
Q

• is triangular in cross-section. A thin vestibular membrane separates cochlear duct from scala vestibuli, presenting an ionic barrier between
perilymph and endolymph
• An osseous spiral lamina and basilar membrane separate cochlear duct from the scala tympani.
• Within the cochlear duct, a spiral organ sits atop the basilar membrane along its entire length from the base to the apex of the
cochlea.

A

cochlear duct (scala media)

127
Q
  • is critical in the physiology of hearing. It consists of radial fibers that extend outward from the osseous spiral lamina. The fibers are shortest and stiffest at the base of the cochlea and they are longest at the apex.
  • it is fixed
A

basilar membrane

128
Q

• features receptor cells (hair cells) arranged along one inner row and three outer rows. Each hair cell has dozens of stereocilia on its free surface. Hair cells are held in place by a reticular membrane (plate) anchored to the basilar membrane. Stereocilia project above the reticular plate, making contact with a tectorial membrane. The tectorial membrane arises from the limbus, a tissue mass set solidly on the osseous spiral lamina.

A

spiral organ (organ of Corti)

129
Q

Auditory Pathway

A

• Cochlear nerve fibers synapse in dorsal and ventral cochlear nuclei, typically each fiber synapses in both nuclei. Thereafter, the auditory pathway is bilateral and complex because of many synaptic possibilities.
• Fibers decussate in the trapezoid body,
the pathway then ascends in the lateral lemniscus and then in the brachium of the inferior colliculus, then in the medial geniculate body, from which neurons send their axons through the internal capsule to cerebral cortex surrounding the sylvian sulcus (primary auditory cortex)

130
Q

• Lesions of cochlear nuclei (or cochlear nerve or a cochlea) produce __

A

unilateral deafness

131
Q

• lesions central to the cochlear nuclei affect __

A

both ears (because central pathways are bilateral)

132
Q

• is present when the sound is not reaching the inner ear, the cochlea. This can be due to external ear canal malformation, dysfunction of the eardrum or malfunction of the bones of the middle ear.
• The ear drum may show defects from small to total resulting in hearing loss of different degree. Dysfunction of the three small bones of the middle ear – malleus, incus, and stapes – may cause conductive hearing loss. The mobility of the ossicles may be impaired for different reasons and disruption of the ossicular
chain due to trauma, infection or anchylosis may also cause hearing loss.

A

Conductive hearing loss

133
Q

Conductive hearing loss: Etiology

A
  • Cerumen
  • Otitis externa
  • Foreign Body in auditory canal
  • Perforated tympanic membrane
  • Otitis media
  • Cholesteatoma
  • Temporal bone trauma
134
Q
  • is one caused by dysfunction of the inner ear, the cochlea, the nerve that transmits the impulses from the cochlea to the hearing center in the brain or damage in the brain.
  • The most common reason for sensorineural hearing impairment is damage to the hair cells in the cochlea.
A

Sensorineural hearing loss

135
Q

Sensorineural Hearing Loss: Etiology

A

Congenital
• Aplasia of the cochlea
• Congenital cholesteatoma
• Congenital Rubella syndrome

Acquired
• Suppurative labyrinthitis
• Meningitis
• Measles
• Ototoxic drugs
• Physical trauma
• Prolonged exposure to loud noises (>90dB)
• Acoutic neuroma
136
Q
  • is a combination of the two

* Chronic ear infection can cause a defective ear drum or middle-ear ossicle damages, or both.

A

Mixed hearing loss

137
Q

• The __ is performed by placing a high frequency (512 Hz) vibrating tuning fork against the patient’s mastoid bone and asking the patient to tell you when the sound is no longer heard. Once they signal they can’t hear it, quickly position the still vibrating tuning fork 1–2 cm from the auditory canal, and again ask the patient to tell you if they are able to hear the tuning fork.

A

Rinne test

138
Q

Rinne test (Results: Normal Hearing)

A

• Air conduction should be greater than bone conduction and so the patient should be able to hear the tuning fork next to the pinna after they can no longer hear it when held against the mastoid.

139
Q

Rinne test (Results: Abnormal Hearing)

A

• If they are not able to hear the tuning fork after mastoid test, it means that their bone conduction is greater than their air conduction. This indicates there is something inhibiting the passage of sound waves from the ear canal, through the middle ear apparatus and into the
cochlea (i.e., there is a conductive hearing loss).
• In sensorineural hearing loss the ability to sense the tuning fork by both bone and air conduction is equally diminished. Sensorineurally hearing loss patients usually can hear better on the mastoid process than air process, but indicate the sound has stopped much earlier than conductive loss patients.

140
Q

Weber test

A

• Tuning fork is placed in the middle of the forehead, or on top of the head equi-distant from the patient’s ears. The patient is asked to
report in which ear the sound is heard louder.
• A normal weber test has a patient reporting the sound heard equally in both sides.
• In an affected patient, if the defective ear hears the Weber tuning fork louder, the finding indicates a conductive hearing loss in the
defective ear.
• In an affected patient, if the normal ear hears the tuning fork sound better, there is sensorineural hearing loss on the other (defective) ear.
• However, the aforegoing presumes one knows in advance which ear is defective and which is normal

141
Q

• Anatomical site: Inner ear,cranial nerveVIII, or central processing centers
• Weber test: Sound localizes to normalear
• Rinne test:
Positive Rinne; air conduction > bone conduction (both air and bone conduction are decreased equally, but the difference between them is unchanged).

A

Sensorineural hearing loss

142
Q
  • Anatomical site: Middle ear(ossicular chain),tympanic membrane, orexternal ear
  • Weber test: Sound localizes to affected ear (ear with conductive loss)
  • Rinne test: Negative Rinne; bone conduction > air conduction (bone/air gap)
A

Conductive hearing loss

143
Q

Rinne both ears: Air Conduction>Bone Conduction

A

• Weber without lateralization: Normal/bilateral
sensorineural loss
• Weber lateralizes left: Sensorineural loss in
right
• Weber lateralizes right: Sensorineural loss in left

144
Q

Rinne left: Bone Conduction>Air Conduction

A
  • Weber lateralizes left: Conductive loss in left

* Weber lateralizes right: Combined loss: conductive and sensorineural loss in left

145
Q

Rinne right: Bone Conduction>Air Conduction

A

• Weber lateralizes left: Combined loss:
conductive and sensorineural loss in right
• Weber lateralizes right: Conductive loss in right

146
Q

Rinne both ears: Bone Conduction>Air Conduction

A
  • Weber without lateralization: Conductive loss in both ears
  • Weber lateralizes left: Combined loss in right and conductive loss on left

• Weber lateralizes right: Combined loss in left
and conductive loss on right

147
Q

Olfactory Receptor

A
  • The olfactory mucosa contains theolfactory receptor neuronsthat are responsible for scent transduction.
  • The transduction occurs in the olfactory receptorslocated on cilia at the ends of the olfactory receptor neurons.
148
Q

Olfactory Pathway (1)

A

• Odorant molecules can reach the olfactory receptors via a passive pathway or an assisted pathway.
*In the passive route, molecules reach the olfactory mucosa via inhaled air.
*In the assisted pathway, the molecules attach to an olfactory binding protein that transports them directly to the olfactory receptors.
• There are about 1,000 kinds of olfactory receptors; all the olfactory receptors are the same on each olfactory receptor neuron.

149
Q

Olfactory Pathway (2)

A
  • Some afferent fibers from the Mitral continue to the anterior olfactory nucleus. The rest simply continue the olfactory tract and cross over
  • From the Anterior Olfactory Nucleus, the fibers continue to the olfactory Trigone where it synapses with 3 different nucleus. The main one will be the Lateral Olfactory
  • Olfactory Trigone and Olfactory Tuberculum to the anterior commissure influencing autonomic centers.
150
Q

• Primary Olfactory Cortex

A

Lateral Olfactory Tract

151
Q

Olfactory Pathway (3)

A

• Olfactory Cortex. - Those portions of the cerebral cortex that receive direct projections
from the olfactory bulb (via mitral cell axons) are collectively referred to as the olfactory cortex. Note the olfactory cortex is the one area of cortex that receives direct sensory input without an inter posed thalamic connection. Most of the olfactory cortex is of a primitive 3-layered type

152
Q

The Olfactory Cortex include

A
  • Anterior Olfactory nucleus
  • Olfactory Tubercle
  • Piriform Cortex
  • Entorhinal Cortex
  • Insular Cortex
  • Amygdala
153
Q

• When testing for olfactory impairment it is necessary to keep two things in mind:

A
  1. The olfactory pathways up to the level of the anterior commissure are completely separate, so each nostril can be tested separately in order to detect a unilateral anosmia;
  2. There are endings of the trigeminal nerve (free nerve endings) within the nasal cavity
    which respond to irritating or pungent odors.
154
Q

• Loss of Smell

A

Anosmia

155
Q

Dysosmia divided into:

A
  1. Troposmia

2. Phantosmia

156
Q
  • distorted quality of an odorant stimulation

* pathophysiology: decreased number of functioning neurons causing incomplete characterization

A

Troposmia

157
Q
  • perceived odor when no odorant is present

* pathophysiology: abnormal signal from the olfactory neurons

A

Phantosmia

158
Q

Olfactory clinical manifestations (1)

A
  • nerve bundles can be severed as a result of skull fractures or other pathology in this region with a resulting partial or complete anosmia.
  • The temporal lobe the olfactory cortex, covers the rostral portion of the parahippocampal gyrus and the uncus. The temporal lobe is known to be a site for seizure, sometimes these seizures are preceded by hallucinations of disagreeable odors, reflecting the olfactory function.
159
Q

Olfactory clinical manifestations (2)

A

• Foster- Kennedy Syndrome

  • Optic atrophy – ipsilateral
  • Papilledema – contralateral
  • Anosmia – ipsilateral
  • Central scotoma – ipsilateral

• Due to optic nerve compression, olfactory nerve compression and increased intracranial pressure

160
Q
  • Limbic is latin word limbus which means border or edge.
  • In the brain, it is the border between the neocortex and the diencephalon.
  • Also known as the Circle of Paper (Papez’s Circuit)
A

Limbic System

161
Q

Functions of the Limbic System

A
  • Feeding (Satiety and hunger)
  • Forgetting (Memory)
  • Fighting (Emotional response)
  • Family (Sexual reproduction and maternal instincts)
  • Fornication (Sexual arousal)
162
Q

Limbic System: Cortical

A
  • Neocortex
  • Orbitofrontal
  • Hippocampus
  • Insular Cortex
  • Cingulate
  • Subcallosal
  • Parahippocampal gyri
163
Q

Limbic System: Subcortical

A
  • Amygdala
  • Olfactory bulb
  • Septal Nuclei
  • Hypothalamus
  • Thalamus
  • Limbic Lobe
164
Q

Limbic Lobe

A
  • Orbitofrontal Cortex
  • Cingulate gyrus
  • Subcallosal gyrus
  • Parahippocampal gyrus
165
Q
  • Small gyrus found anterior to the laminal terminalis and anterior commissure
  • Inferior to the rostrum of the corpus callosum
  • It is believed to be involved in depression
A

Subcallosal Gyrus

166
Q
  • Appreciated while visualizing the medial aspect of the cerebral hemisphere
  • It is believed to be strongly associated with perception of neuropathic pain and nociception
A

Cingulate gyrus

167
Q
  • Almond shaped located anterosuperiorly to the temporal horn of lateral ventricle and deep to the uncus
  • Communication between amygdala and regions of the hypothalamus regulate fear and anxiety responses
A

Amygdala

168
Q

• Umbrella term used to describe a cluster of structures
- Hippocampus
- Dentate gyrus
- Subicular Complex
- Entorhinal Cortex
• Posteriorly the hippocampus merge with the crus of the fornix
• The hippocampus shares the responsibility of transforming short term to long term

A

Hippocampal formation

169
Q

• Function: Formation of long
term memories
• Lesion: Cannot build new memories. Everything she experience fades away
and old memories before damage are untouched

A

Hippocampus

170
Q

• Function:
- Involved in signalling the cortex of stimuli related to being pleasant or unpleasant.
- Formation and storage of memories associated with emotional events
• Lesion: Social and emotional deficits

A

Amygdala

171
Q
  • Function: Process of recognition memory (recollection memory)
  • Lesion: Amnesic syndromes
A

Mammilary Body

172
Q
  • Function: Carries signals from hippocampus to mamillary bodies and septal nuclei
  • Lesion: Memory impairment
A

Fornix

173
Q

• Function: play a role in reward and reinforcement along with the nucleus accumbens. Considered a pleasure zone in animals.

A

Septal nuclei

174
Q
  • Function: Formation of spatial memory (encoding and recognition of scenes rather than faces or objects)
  • Lesion: syndrome in which patients cannot visually recognize scenes even though they can recognize the individual objects in the scenes
A

Parahippocampal gyrus

175
Q

• Function: Autonomic functions regulating heart rate, blood pressure, cognitive and attention processing

A

Cingulate gyrus

176
Q

• Function: Important memory and associative components

A

Entorhinal cortex

177
Q

• Function: Relates to the olfactory system

A

Piriform cortex

178
Q

• Function: Required for decision making

A

Orbitofrontal cortex

179
Q

Cerebral Arteries

A
  • Anterior Circulation: from the Internal Carotid Artery

* Posterior Circulation: from the Basilar Artery

180
Q
  • The anterior communicating artery joins the two ACA’s
  • The posterior communicating arteries join the ICA with the basilar circulation
  • Normally these communicating arteries have little blood flow unless occlusion in one artery occurs;
A

Circle of Willis

181
Q

Circle of Willis (Variants)

A

• The complete circle is seen in only 20 – 25% of individuals
• One or both Pcom’s are hypoplastic in 34%
• The precommunicating segment of ACA (A1) may be absent or hypoplastic (25%)
Bilateral hypoplastic P1 segments (11%)

182
Q

Cerebral veins drain into dural venous sinuses which eventually empty into the __

A

internal jugular vein

183
Q

Dural venous sinuses:

A
  • Superior sagittal sinus
  • Inferior sagittal sinus
  • Sigmoid sinus
  • Straight sinus
  • Transverse sinus
  • Cavernous sinus
184
Q

Major cerebral veins

A
  • Great cerebral vein of Galen
  • Basal vein of Rosenthal
  • Internal cerebral vein
185
Q

1891 - Lumbar puncture was introduced by __

A

Quincke

186
Q

1912 - __ made the first correlations between disease processes and the cellular and chemical changes in the CSF

A

Mestrezat

187
Q

1937 - __ published their classic monograph on the CSF changes in all types of disease

A

Merritt and Fremont-Smith

188
Q

1950s - __ techniques were introduced

A

membrane filtration

189
Q

The studies of Dandy (1919) and of Weed (1935) provided the basis of our knowledge of __ formation, circulation, and absorption

A

Cerebrospinal Fluid (CSF)

190
Q

Cerebrospinal Fluid

A

• The total CSF volume in the adult is ~150 ml
- approximately 30 ml is in the spinal subarachnoid space
• About 500 ml of cerebrospinal fluid is produced per day

191
Q

Functions of the CSF

A

• Mechanical support

  • Provides “water jacket” for the brain and spinal cord
  • Provides buoyancy to the brain

• Removes the waste products of cerebral metabolism
- CO2, lactate, and hydrogen ions

• CSF helps to preserve a stable chemical environment for neurons and their myelinated fibers

192
Q

CSF: Formation (1)

A

• Average rate of CSF formation is 21-22 mL/h (0.35 mL/min)
- approximately 500 mL/day
- The CSF as a whole is therefore renewed four or five times daily
• The choroid plexuses, located in the floor of the lateral, third, and fourth ventricles, are the main sites of CSF formation

193
Q

CSF: Formation (2)

A

• The thin-walled vessels of the plexuses allow passive diffusion of substances from the blood plasma into the extracellular space surrounding choroid cells

  • Electrolytes equilibrate with the CSF at all points in the ventricular and subarachnoid spaces
  • The same is true of glucose
  • The transport of sodium is accomplished by the action of a sodium-potassium-ion exchange pump at the apical surface of the choroid plexus cells
194
Q

CSF: Formation (3)

A
  • It is also known that the penetration of certain drugs and metabolites is in direct relation to their lipid solubility
  • Ionized compounds, such as hexoses and amino acids, being relatively insoluble in lipids, enter the CSF slowly unless facilitated by a membrane transport system
195
Q

Blood-CSF and Blood-Brain Barrier

A

• The term blood–brain barrier (BBB) is a collective term for all barriers lying between the plasma and the neuropil
- one of which is the blood–CSF barrier (BCB)
• BBB is formed by the tight junction (zonula occludens) of capillary endothelial cells
• Physiologically, the system of barriers enables the regulation of the osmolarity of brain tissue and CSF and the intracranial pressure and volume

196
Q

Blood-CSF and Blood-Brain Barrier 2

A

• Biochemically, the BCB is permeable to water-soluble substances but not to lipo-soluble substances such as anesthetics, psycho- active drugs, and analgesics
- The BBB, on the other hand, is generally permeable to liposoluble substances (of molecular weight less than 500 daltons) but not to water-soluble substances.

197
Q

Specialized Areas without BBB

A
  • Vascular Organ of the Lamina Terminalis
  • Area postrema
  • Median eminence
  • Pineal body
  • Posterior pituitary
  • Subfornicial organ
198
Q

Cerebral Ventricles and CSF Circulation

A

• The fluid-filled cerebral ventricles constitute the inner CSF space

  • two lateral ventricles communicates with the third ventricle through the interventricular foramen of Monro
  • Fluid passes from the third ventricle through the cerebral aqueduct (of Sylvius) into the fourth ventricle
  • through the single midline foramen (of Magendie) and paired lateral foramina (of Luschka) into the subarachnoid space (outer CSF space).
199
Q

Cisterns

A
  • Cisterna magna - cerebellomedullary
  • Pontine cisterns
  • Interpeduncular cisterns
  • Chiasmatic cisterns
  • Superior cisterns `
200
Q

– from the conus medullaris to about the 2nd sacral

vertebra; contains the filum terminale and nerve roots of cauda equina

A

Lumbar cistern

201
Q

CSF: Circulation

A
  • The pressure is highest in the ventricles and diminishes successively along the subarachnoid pathways
  • Arterial pulsations of the choroid plexuses help drive the fluid from the ventricular system
202
Q

CSF: Absorption

A

• Absorption of CSF is through the arachnoid villi

  • microscopic excrescences of arachnoid membrane that penetrate the dura and protrude into the superior sagittal sinus and other venous structures
  • form the pacchionian granulations or bodies
  • The arachnoid villi are present at the base of the brain and around the spinal cord roots and have been thought to act as functional valves that permit unidirectional “bulk flow” of CSF into the vascular lumen
203
Q

CSF Volume and Pressure

A

• ICP and consequently CSF pressure measured by lumbar puncture is normally about 8 mmHg or 110 mmH2O
(1 mmHg equals 13.7 mmH2O)

204
Q

(CSF Volume and Pressure)

The inhalation or retention of CO2 raises the blood PCO2 and correspondingly decreases the pH of the CSF

A

This acts as a potent cerebral vasodilator, causing an increase in cerebral blood flow and leading to intracranial hypertension

205
Q

(CSF Volume and Pressure)

Hyperventilation, which reduces PCO2, has the opposite effect

A
  • It increases the pH and the cerebral vascular resistance and thereby decreases CSF pressure
  • This maneuver of lowering the arterial CO2 content is utilized in the treatment of acutely raised ICP.
206
Q

(CSF Volume and Pressure)

Increased venous pressure exerts an almost immediate effect on CSF pressure by increasing the volume of blood in the cerebral veins, venules, and dural sinuses

A
  • If jugular veins are compressed, there is a rise of intracranial pressure that is transmitted to the lumbar subarachnoid space
  • This is the basis of the Queckenstedt test
207
Q

CSF Volume and Pressure 2

A
  • The Valsalva maneuver also causes an increased intra-thoracic pressure, which is transmitted to the jugular and then to the cerebral and spinal veins
  • The ICP rises in heart failure, when central and jugular venous pressures become elevated
  • Mediastinal tumors, by obstructing the superior vena cava, have the same effect
208
Q

(Increased Intracranial Pressure)
1. The intact cranium and vertebral canal, together with the relatively inelastic dura, form a rigid container, such that an increase of any of its contents—brain, blood, or CSF—will elevate the ICP

  1. Furthermore, an increase in volume of any one of these three components must be at the expense of the other two,
A

Monro-Kellie Doctrine

209
Q

Cerebral Perfusion Pressure Formula

A

CPP = MAP – ICP

CPP Cerebral Perfusion Pressure
MAP Mean Arterial Pressure
ICP Intracranial Pressure

210
Q

Cycle of Increase ICP

A

Decrease CCP&raquo_space; Disrupt cellular metabolism&raquo_space; Disruption of osmotic gradient&raquo_space; Influx of water in cell&raquo_space; Increase ICP&raquo_space; Decrease CCP

211
Q

Causes of Increased ICP

A
  1. A cerebral or extracerebral mass
  2. Generalized brain swelling,
  3. An increase in venous pressure
  4. Obstruction to the flow and absorption of CSF
  5. Any process that expands the volume of CSF
212
Q

Increased ICP: Clinical Features

A
  • Headache
  • Nausea and vomiting
  • Drowsiness
  • Ocular palsies
  • Papilledema
213
Q
  • After several days or longer, papilledema may result in periodic visual obscurations
  • If papilledema is protracted, optic atrophy and blindness may follow
A

Papilledema

214
Q

• A condition in which there is ventricular enlargement under tension as a result of an obstruction to the flow of CSF at some point in its ventricular pathway

  • aqueduct of Sylvius
  • medullary foramens of exit (Luschka and Magendie)
  • basal subarachnoid space.
A

Hydrocephalus

215
Q

• Because of the obstruction, CSF accumulates within the ventricles under increasing pressure, enlarging the ventricles and expanding the hemispheres

A

Hydrocephalus

216
Q

Clinical Picture: Acute Hydrocephalus

A
  • Headache of varying severity
  • Vomiting
  • Becomes drowsy or stuporous
  • Bilateral Babinski signs are the rule
217
Q

Clinical Picture: Acute Hydrocephalus (Eyes)

A

Early in the process, the pupils are normal in size and the eyes may rove horizontally; as the ventricles continue to enlarge, the pupils become miotic, the eyes then cease roving and assume an orthotopic position, or there may be bilateral abducens palsies and limitation of upward gaze

218
Q

Clinical Picture: Acute Hydrocephalus (2)

A
  • In the advanced stages, which are associated with coma, there is increased tone in the lower limbs and extensor posturing
  • CNS infection/ Meningitides
  • Subarachnoid hemorrhage
  • Trauma
219
Q
  • There is frontal bossing and the skull tends to be brachiocephalic
  • With marked enlargement of the skull, the face looks relatively small and pinched and the skin over the cranial bones is tight and thin, revealing prominent distended veins
A

CONGENITAL HYDROCEPHALUS

220
Q

Clinical Picture: Chronic Hydrocephalus

A
  • The infant is fretful, feeds poorly, and may vomit frequently
  • The infant appears languid, uninterested in his surroundings, and unable to sustain activity
  • Later it is noticed that the upper eyelids are retracted and the eyes tend to turn down; there is paralysis of upward gaze, and the sclerae above the irises are visible - setting-sun sign
221
Q

Causes of this disorder (chronic hydrocephalus) are :

A

(1) intraventricular matrix hemorrhages in premature infants
(2) fetal and neonatal infections
(3) type II Chiari malformation
(4) aqueductal atresia and stenosis
(5) the Dandy-Walker syndrome.

222
Q

(OCCULT HYDROCEPHALUS)

  • patient may complain of bifrontal or bioccipital headaches
  • Symptoms and signs are predominantly those of a frontal lobe disorder of mentation or of gait
  • Slowness of mental response (abulia), inattentiveness, distractibility, perseveration, and inability to plan activity or to sustain any type of complex cognitive function are characteristic
A

Normal Pressure Hydrocephalus

223
Q

(OCCULT HYDROCEPHALUS)

  • Memory may be slightly impaired
  • Gait deteriorates early in the course of hydrocephalus
  • A suck reflex and grasp reflexes of the hands and feet are variably present; plantar reflexes are sometimes extensor
  • There may be sphincteric incontinence
A

Normal Pressure Hydrocephalus

224
Q

CNS infection may involve:

A
  • eptomeninges and CSF spaces (meningitis)
  • ventricular system (ventriculitis)
  • gray and white matter of the brain (encephalitis)
  • the spinal cord (myelitis)
225
Q

Clinical Picture: Meningitis

A
  • fever
  • severe headache and backache
  • photophobia and phonophobia
  • nausea, vomiting
  • impairment of consciousness
  • stiff neck and hyperextended posture, with opisthotonus
226
Q

• in the supine position the patient can easily and completely extend the leg; in the sitting posture or when lying with the thigh flexed upon the abdomen the leg cannot be completely extended; it’s positive

A

Kernig’s sign

227
Q

• A physical sign of meningitis, which is evoked by either passive flexion of one leg, resulting in a similar movement on the opposite side, or if the neck is passively flexed and flexion occurring in the legs.

A

Brudzinski sign

Neuroscience (8 decks)

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