Case 16 Flashcards
Uncal herniation is caused by…
Raised intracranial pressure
Uncal herniation
Uncus (medial edge of temporal lobe) forced below tentorium cerebelli to compress the midbrain.
Signs of uncal herniation
Abnormal posture
Poor GCS
Eye down and out, enlarged ipsilateral pupil and absent light reflex (compression of CNIII)
Potential coma (compression of midbrain)
Central/Trans Tentorial Herniation
Entire brain moving downward.
Can see symmetric downward movement of thalamic structures.
Compression of upper midbrain, therefore affecting pons and medulla as well.
Signs of Central/Trans Tentorial Herniation
Diabetes insipidus (compression of pituitary stalk)
Dilated fixed pupils.
Paralysis of upper eye movement (AKA sunset eyes)
False localising sign.
Most common brain herniation
Cingulate/Subfalcine/Transfalcine
Cingulate/Subfalcine/Transfalcine Herniation
Displacement of brain (typically cingulate gyrus) under falx cerebri, across midline
Signs of Cingulate/Subfalcine/Transfalcine Herniation
Few signs since brainstem relatively preserved.
Contralateral obstructive hydrocephalus (due to obstruction of interventricular foramen between lateral and 3rd ventricles)
Contralateral leg weakness (compression of anterior cerebral artery)
Foramen of Monroe
Interventricular foramen between lateral ventricles and 3rd ventricle.
Foraminal/Tonsillar Herniation
Downward herniation of cerebellar tonsils into foramen magnum.
Signs of Foraminal/Tonsillar Herniation
Respiratory arrest (compression of respiratory centre in medulla)
Instant deterioration
No other signs since structures superior to medulla are unaffected.
Vertebral arteries arise from…
Subclavian arteries
Vertebral arteries fuse to form…
Basilar artery
Blood supply to brainstem
Vertebral and basilar arteries.
Therefore, strokes involving these arteries have a high mortality (85%) since brainstem controls life support functions.
Ascending Reticular Activating System (ASAS) controls…
Consciousness
Consists of many components in brainstem - damage results in coma.
Signs/Symptoms of damage to spinothalamic tract
Contralateral loss of pain and temperature sensation on the body
Signs/Symptoms of damage to trigeminal tract
Ipsilateral loss of pain/temperature sensation on the face
Nucleus Ambiguus
Located in medullary reticular activating system.
Innervation of muscles of soft palate, pharynx and larynx
Signs/Symptoms of damage to Nucleus Ambiguus and Nerve roots of CNIX and X
Dysphagia
Hoarseness
Loss of gag reflex
Lateral medullary syndrome is caused by
Occlusion of Posterior Inferior Cerebellar Artery
Signs/Symptoms of damage to Hypothalamospinal Fibres (Dorsal Longitudinal Fasciculus
Ipsilateral Horner’s Syndrome
Signs/Symptoms of damage to Vestibular Nuclei
Vetigo
Tendency to fall to ipsilateral side
Diplopia (double vision)
Signs/Symptoms of damage to spinocerebellar tract
Ipsilateral ataxia
Cause of lateral medullary syndrome
PICA occlusion
PICA
Posterior Inferior Cerebellar Artery
Signs/Symptoms of Lateral Medullary Syndrome
Contralateral loss of pain and temp sensation on the body.
Ipsilateral loss of pain and temp sensation on the face.
Dysphagia/Hoarseness/Loss of gag reflex
Ipsilateral Horner’s Syndrome
Vertigo/falling to ipsilateral side/ diplopia
Ipsilateral ataxia
Spinal tracts affected by lateral medullary syndrome
Spinothalamic tract Trigeminal Tract Nucleus Ambiguus and roots of CNIX and X Hypothalamospinal Fibres Vestibular Nuclei Spinocerebellar Tract
Glial cell division occurs…
Throughout life
Neuronal cell division occurs…
Before birth
Brain cells found in brain tumors
Glial cells (glioma)
OR
Cells of meningeal coverings (Meningioma)
Function of Microglia
Attack disease organisms and phagocytose damaged cells
Function of oligodendrocytes
Myelination
Schwann cells of the CNS.
Necrosis
Loss of membrane integrity, resulting in release of inflammatory mediators which can cause further damage.
Apoptosis
Programmed cell death.
Cell breaks up into membrane bound bodies containing intact organelles.
No release of inflammatory mediators.
Cellular changes resulting in apoptosis
Loss of trophic factors needed for cell survival - BDNF and NGF.
Extracellular ligands e.g. TNF
Apoptosis is orchestrated by…
Proteolytic enzymes called caspases
DNAases
Galectin-1
Factor secreted by macrophages that promotes Schwann Cell migration and axon regrowth following axonal injury.
Function of Schwann cells in axonal regeneration
Phagocytose debris
Secrete trophic factors to promote axonal growth.
Function of Calpain in axonal regeneration
Breakdown of cytoskeleton
Function of macrophages in axonal regeneration
Secrete factors (e.g. Galectin-1) that promote axon regrowth and schwann cell migration
Function of microglia in Glial Scar formation
Removal of debris
Function of Astrocytes in Glial Scar Formation
Begin to divide and hypertrophy 48 hrs after injury.
Reform a barrier to the brain by linking of their processes together around the lesion.
Function of Meningeal-like cells in Glial Scar Formation
Invade the lesion cavity to form a plug
Cytokines involved in Glial Scar formation…
Released by…
IL-6, TGF-beta, FGF-2
Microglia, neurons and astrocytes
Key cell in Glial Scar Formation
Astrocytes
Why does axonal regrowth not occur in CNS?
Astocytes produce Chrondroitin Sulphate Proteoglycans (CSPGs) e.g. Versican
Oligodendrocytes release NogoA (also transition from CNS to PNS when oligodendrocytes are replaced by Schwann cells, acts as an inhibitor)
Diffuse axonal injury
A shearing injury causing extensive lesions in white matter tracts occurring over a widespread area.
Results in immediate unconsciousness
Why does unconsciousness occur?
Functional disturbance in Ascending Reticular Activating system (responsible for consciousness and arousal)
Protein associated with DAI
Beta-amyloid protein, accumulates 2-3 hours post injury
Petechial Haemorrhages in the brain
Small sources of blood leakage at the interface of grey and white matter.
Assoc w/ DAI
Indicative of severe brain injury.
(Looks like white spots on CT brain scan)
White matter haemorrhage due to DAI can result in…
Complete loss of corpus callosum and enlargement of ventricles.
Function of Nerve Growth Factor and Brain-Derived Neurotrophic Factor
Released at synapses. Maintain and promote survival of neurons.
Transneuronal Degeneration
Degeneration of axons adjacent to injured axon.
Occurs since NGF and BDNF (supporters of neuronal survival) are no longer released from injured axon at its synapses.
Therefore, apoptosis of neurons it contacts.
Why does extracellular [Glutamate] rise in traumatic brain injury?
Rupture of axons causing release of glutamate.
Anaerobic metabolism by astrocytes resulting in acidity and therefore, reduced reuptake of glutamate.
Cellular Consequences of Excitotoxicity
Activating of AMPA and NMDA receptors by glutamate causes increased intracellular Ca2+
Activation of calpains, proteases, phospholipases and endonucleases resulting in cell necrosis.
Ca2+ also causes activation of proapoptotic genes e.g. caspases
Molecules responsible for prevention of oxidative stress
Reactive oxygen species produced in oxidative phosphorylation by mitochondria.
Mopped up by vitamins A and E, superoxide dismutase, catalase and glutathione peroxidase.
Why does excitotoxicity result in oxidative stress?
High Ca2+ which must be sequestered by mitochondria.
Mitochondria work harder therefore producing more ROS.
Too much ROS for antioxidants to mop up.
ROS cause oxidation and malfunction of important molecules
Symptoms of Meningitis
Headache, fever, stiffness (TRIAD)
+
Photophobia
Altered consciousness
Seizures
Non blanching rash
Signs of Bacterial Meningitis
Headache, fever and neck stiffness (TRIAD)
Altered consciousness, low blood pressure, petechial rash, tachycardia.
How does viral meningitis differ from bacterial meningitis clinically?
Viral is less severe, often self-limiting.
Viral causes high fever but BP remains normal and there is no rash.
Causes of RBCs in CSF
Traumatic Tap
Intrathecal bleeding
How do you distinguish between traumatic tap and intrathecal bleeding in CSF examination?
Traumatic tap - RBC count will decrease in number across multiple samples.
Intrathecal bleeding - RBC count is consistent across multiple samples.
Xanthochromia
Yellow tinge in CSF samples after blood products have been present for 12hrs
> 90% polymorphs (neutrophils in CSF
Bacterial infection
> 90% lymphocytes in CSF
Viral infection
Normal white cell count in CSF
No white cells is NORMAL.
<5 is acceptable unless there is sufficient history
CSF in bacterial meningitis
Yellowish, turbid
Increased polymorphs
Increased proteins
Decreased glucose
Normal lymphocytes
CSF in viral meningitis
Clear fluid
Increased lymphocytes
Normal lymphocytes, protein and glucose
Bacterial causes of meningitis
Neisseria Meningitidis (Gram -ve) Streptococcal pneumoniae (Gram +ve) Listeria Monocytogenes (Gram +ve)
Viral cause of meningitis
Enterovirus
Treatment of bacterial meningitis
Broad spectrum antibiotics initially: Ceftriaxone (+ Ampicillin if Listeria suspected i.e. pregnant or elderly)
Continue Abx until CSF results are unequivocal.
Tx adjuncts e.g. Dexamethasone in S.Pneumoniae
Monitor GCS (GCS<7 means airway is probably compromised)
Check clotting
Treatment for viral meningitis
Analgesia
Antiemetics
Hydration
When is a CT scan of head indicated in meningitis?
Raised ICP
Immunocompromised
Reduced GCS
Chronic Meningitis
TB and cryptococcal meningitis.
Often presents with cranial neuropathy since inflammation occurs at base of skull.
Causes little or no pain.
Travel Hx is very important here
CSF in fungal meningitis
Yellow and viscous
Increase lymphocytes
Protein and polymorphs may be increased or normal
Glucose may be decreased or normal.
Symptoms of encephalitis
Headache
Seizure
Personality change
Neurological signs
(May first present in psychiatric services)
Causes of encephalitis
Herpes Simplex CMV EBV Varicella Zoster HIV Enterovirus Measles Virus
Can also be autoimmune
Treatment of viral encephalitis
Aciclovir
or HAART if secondary to HIV/AIDS
MOA of Aciclovir
DNA polymerase inhibitor.
Inhibits DNA synthesis by virus.
Karposi Sarcoma
Tumour caused by Human Herpes Virus 8 - lesions in skin, mucus membranes and lymph nodes due to poor control of HIV
Vacuolar Myelopathy
Associated with low CD4+ lymphocytes in HIV.
Symptoms include:
Painless leg weakness, stiffness, sensory loss, imbalance, sphincter dysfunction
Paralytic Poliomyelitis
Occurs in 2% of poliomyelitis.
Anterior horn cells in spinal cord are attacked causing asymmetric flaccid paralysis in one or more limbs.
Since this usually occurs in childhood, limb does not grow to full size.
Cause of intracerebral abscess/empyema
Local infection (e.g. mastoid air cells, venous sinuses, otitis media) that spreads intracranially
Symptoms of rabies
Hypersalivation Perspiration Pupillary dilatation Priapism - persistent and painful erection of penis) Fever Agitation Depression Foaming at mouth after drinking due to throat spasms
Fatal when symptomatic
Virus which causes rabies
Lyssavirus
Negri bodies
Eosinophilic, sharply outlined bodies found in cytoplasm of neurons infected with lyssavirus (rabies). Especially pyramidal cells within Ammon’s horn of the hippocampus.
Treatment of rabies
Hospitalisation
Immunoglobulin treatment
Anti-rabies vaccine
Symptoms of tetanus
Spasms and stiffness in jaw muscles (trismus/lock jaw)
Stiffness of neck and abdominal muscles
Difficulty swallowing
Painful body spasms (last several minutes)
How does Botulinism manifest in the body?
Clostridium botulinism is a bacteria found in soil and canned foods.
Secretes botulinum toxin (botox) which causes symptoms of botulinism when ingested.
Signs/Symptoms of Botulinism
Descending paralysis including respiraory failure. Blurred vision Pupil dilatation Nausea Diarrhoea
Treatment of botulinism
Intubation
Antitoxin
Most common parasitic disease of CNS
Taenia Solium - cysticercosis
Most common cause of epilepsy worldwide
Cysticercosis - Taenia Solium parasite infection
Signs/Symptoms of Cysticercosis
New onset of seizures +/- raised ICP if CSF flow is interrupted
Treatment of cysticercosis/Taenia Solium
Praziquantel or Albendazole - used n treatment of parasitic worm infections
Bacteria responsible for neurosyphilis
Treponema Pallidum
Manifestations of Tertiary Syphilis
Neurosyphilis
Gumma
Aortitis/Aortic regurgitation
Latency of neurosyphilis
Pure meningeal = 1yr
Meningovascular = 5-10yrs
Spinal cord involvement =20yrs
Treatment of syphilis
Penicillin
Probenicid
Prion disease of CNS
85% caused by Sporadic Creutzfeldt-Jakob
Brain damage leading to rapid decrease of movement and mental function.
Signs and symptoms of Prion Disease of CNS
Neurodegenerative: Dementia Seizures Personality change Ataxia Startle myoclonus (sudden muscle contraction)
Metabolic causes of coma without neurological signs
Hyper/Hypoglycaemia Hypoxia Acidosis Thiamine Deficiency Hepatic or Renal Failure Hypercapnia Hypoadrenalism
Most common category of coma
Coma without neurological signs
Toxins resulting in Toxin-Induced Coma without neurological signs
Drugs - benzodiazepines, Barbiturates, opiates, TCAs
Alcohol
Non metabolic, non toxic causes of Coma without neurological signs
Infectious e.g. encephalitis
Vascular e.g. hypertensive encephalopathy
Trauma e.g. concussion
Epilepsy (postictal - after a seizure)
Temperature regulation i.e. hypo/hyperthermia
Causes of coma with neurological signs
Haemorrhage
Infarction
Tumours
Infectious (abscess)
Causes of coma in meningitic syndrome
Subarachnoid haemorrhage
Bacterial meningeal infection
Tentorium
Outgrowth of dura mater, separating cerebellum and cerebrum
Components of reticular formation
Diencephalon (consists of thalamus, hypothalamus and pituitary gland, effectively enclosing the 3rd ventricle)
Midbrain
Rostral pons
Components of reticular activating system
Reticular formation
Thalamus
Cerebral hemispheres
Symptoms of raised ICP
Headache* N+V* Altered consciousness (GCS) Ophthalmoparesis (CNIII, IV and VI affected) Increased systolic and pulse pressure Bradycardia Abnormal respiratory pattern Papilloedema (Chronic only)
*Triad symptoms
False localising sign in raised ICP
CNVI compression - signs do not indicate location of the problem.
Cheyne-Stokes Respiration
Progressively deeper and faster breathing followed by a decrease that results in temporary apnoea.
Caused by bihemispheric damage(cerebellar and thalamic). Usually metabolic origin.
Usually seen in palliative care.
Kussmaul Respiration
Deep and laboured breathing associated with metabolic acidosis (e.g. DKA)
Apneusis
Deep gasping inspiration with a brief pause at full inspiration, followed by a brief insufficient release.
Caused by a lesion in respiratory centre (lateral tegmentum of pons)
Ataxic breathing
Complete irregularity of breathing.
Caused by damage to medulla oblongata.
Apneustic centre
Located in pons
Controls rhythm of breathing
Pneumotactic centre
Located in pons
Controls rate and depth of breathing
Inhibits apneustic centre
GCS: Best eye opening response
Spontaneously 4
To verbal stimuli 3
To painful stimuli 2
None 1
GCS: Best Verbal response
Oriented 5 Confused 4 Inappropriate words 3 Incomprehensible 2 No verbal response 1
Best motor response
Obeys commands 6 Localises pain 5 Withdraws to pain 4 Flexion to pain 3 Extension to pain 2 None 1
Divergence of eyes in the unconscious patient
Normal during drowsiness,
Ocular axes become parallel as coma deepens i.e. drift back to middle.
Conjugate Roving
Deviation of both eyes to one side in the unconscious patient.
Frontal lobe lesion - eyes deviate to ipsilateral side.
Brainstem lesion - eyes deviate to contralateral side
Ocular bobbing
Brisk downward movement of eyes, slow movement back up to primary position.
Caused by damage to PONS bilaterally
Small, reactive pupils in the unconscious patient
Damage to diencephalon (thalamus, hypothalamus and 3rd ventricle)
Drugs
Metabolic encephalopathy
Large, fixed pupils in the unconscious patient
May show hippus (spastic contraction)
Pretectum area of midbrain damaged
Pretectum of midbrain is responsible for…
Constriction of pupil
In the unconscious patient, one eye has a normal pupil, the other is dilated and fixed.
CN III compression
e.g. Uncal Herniation
In an unconscious patient, pupils are in the midposition and fixed size
Midbrain damaged
In an unconscious patient, pupils are very small (pinpoint)
Pons damaged
In what order are eye reflexes lost in the unconscious patient
First, reflex eye movements
Second, corneal reflex
Third, pupillary reflex to light
Vestibulo-ocular reflex
When head rotates to one side, the eyes move to the other
Vestibulo-ocular reflex assesses function of…
Medial longitudinal fasciculus in brainstem - main centre of connection for CN III, IV and VI
When turning the head of an unconscious patient (Doll’s eye manoeuvre), the eyes move to the ipsilateral side. Area of damage is?
Medial longitudinal fasciculus in brainstem
Normal result in caloric testing
Eyes deviate to side of unpleasant stimulus AND nystagmus
Caloric testing
Irrigation of one ear with 20ml of cold water. Eye movements are assessed.
On carrying out a caloric test on an unconscious patient, there is no nystagmus in both eyes. This indicates…
Low brainstem lesion
On carrying out a caloric test on an unconscious patient, there is no nystagmus in one eye. This indicates…
Medial Longitudinal Fasciculus lesion
Unconscious patient with hypertonia
Established (long term) damage to cortex or proximal cervical spine.
Unconscious patient with flaccid paralysis
Acute spinal cord injury
Hypertonia develops over time
Decorticate posturing of unconscious patient
Arms adducted, flexed at the elbow and wrist.
Caused by damage to one or both corticospinal tracts
Decerebrate posturing of unconscious patient
Arms adducted, extended at the elbow, pronated and flexed at the wrist.
Caused by damage to upper brainstem
Precentral gyrus contains
Primary motor cortex
Arrangement of primary motor cortex
Leg closest to midline.
Face most lateral
PMC is found in which lobe?
Frontal lobe
Broca’s Area
Motor speech centre in frontal lobe
Arrangement of primary sensory cortex
Leg closest to midline.
Face most lateral
Occipital lobe contains
Visual cortex
Temporal Lobe functions
Contains primary auditory cortex - involved in hearing. Involved in formation of new memories and interpretation of visual stimuli Language comprehension (contains Wernicke's Area)
Location of insular lobe
Deep to lateral surface of brain (underneath frontal, parietal and temperal lobes.
Function of insula
Primary gustatory cortex language visual-vestibular integration Sympathetic tone Perception, motor control, self awareness and cognitive functioning
Damage to insula is associated with
arrhythmias
Basal ganglia
Lentiform nucleus (Globus pallidus and Putamen)
Caudate nucleus
Substantia nigra
Subthalamic nuclei
Function of lentiform nuclei
Regulation of movement
Function of caudate nucleus
Memory and learning
Corpus striatum consists of…
Lentiform nucleus (Globus pallidus and Putamen) Caudate nucleus
Function of thalamus
Relay of sensory information to cortex.
Sleep, wakefulness, consciousness and arousal.
Thalamus is supplied by…
Posterior cerebral artery
Corona Radiata in the brain
White matter tract which is an extension of internal capsule, carrying ascending and descending fibres.
Most common sites of intracranial aneurysm
Anterior communicating (40%) Bifurcation of middle cerebral (34%) Posterior communicating (20%) Basilar Tip (4%)
Arterial supply of Caudate nucleus
Anterior cerebral artery
Arterial supply of Lentiform nucleus
Middle cerebral artery
Arterial supply of thalamus
Posterior cerebral artery
Arterial supply of internal capsule
Anterior choroidal artery
Torcular Herophili
Confluence of sinuses of the cerebrum
Venous sinuses of cerebrum drain into…
Internal jugular vein
Foramen of Monro
Connects lateral ventricles to the 3rd ventricle
Sylvian Aqueduct
Connects 3rd and 4th ventricle
Foramen of Luschka
Links 4th ventricle to cerebellopontine cistern. Allows CSF to enter subarachnoid space.
Foramen of Magendie
Links 4th ventricle and foramen magnum. Allows CSF to enter subarachnoid space.
Lobes of cerebellum
Anterior (petrosal)
Superior (tentorial)
Inferior (suboccipital)
Function of cerebellum
Coordination and timing of movements
Where is the cerebellum situated?
Posterior cranial fossa, behind 4th ventricle, pons and medulla.
Tentorium cerebelli
Separates cerebellum from cerebrum
Components of midbrain
Tectum
Tegmentum
Cerebral peduncles (containing ascending and descending tracts to and from cerebrum)
Arterial supply of pons
Superior cerebellar artery
Pontine branches of basilar artery
Ventral pons contains
White matter tracts: Corticospinal and corticobulbar
Which cranial nerves arise from Dorsal Tegmentum of Pons?
CNV, VI, VII and VIII
Mesencephalon
Midbrain
Metencephalon
Pons
Myencephalon
Medulla Oblongata
Corticobulbar tract
Supplies muscles of head and neck
Bulbar reflexes
Coughing, sneezing, swallowing and vomiting
Medulla Oblongata contains…
Autonomic cardiovascular and respiratory centres - controls breathing, blood pressure and heart rate
Reflex centres for bulbar reflexes e.g. vomiting and sneezing
Arterial supply to medulla oblongata
PICA
Anterior spinal artery
Vertebral arteries
Ventral/Anterior medulla oblongata contains…
Olive
Pyramidal tracts (e.g. corticospinal)
CN IX-XII rootlets
Tegmentum/Dorsal medulla oblongata contains…
CN nuclei
White matter tracts
Decussation of pyramids occurs in the…
Medulla oblongata
Prevertebral soft tissue spaces seen on a lateral C-Spine X-Ray
C1 Nasopharyngeal
C2-4 Retropharyngeal
C5-7 Retrotracheal
Normal size for C1 Nasopharyngeal space on a lateral C-Spine X-Ray
<10mm
Normal size for C2-4 Retropharyngeal space on a lateral C-Spine X-Ray
<5-7mm
Normal size for C5-7 Retrotracheal space on a lateral C-Spine X-Ray
<22mm (or <14mm in children)
Mechanism for Hangman’s Fracture
Hyperextension (e.g. hanging, chin hitting dashboard in car accident)
What is a Hangman’s Fracture?
Fracture through pedicle of the axis
Radiographic features of a Hangman’s Fracture
Prevertebral swelling
Anterior dislocation of the C2 vertebral body
Bilateral C2 pedicle fractures
Radiographic features of bilateral facet dislocation
Complete anterior dislocation of affected body by half or more of the vertebral body AP diameter
Management of brain contusion
Observe for signs of raised ICP (craniotomy/ectomy for persistently raised ICP)
Prevent hypoxia and hypotension
Craniectomy
Removal of part of skull to allow a swelling brain to expand
Craniotomy
Surgical removal of part of skull to expose part of brain
Cause of depressed skull fracture
Impact with a sharp edge e.g. brick, hammer
Management of depressed skull fracture
Usually conservative
Clean and suture overlying lacerations (especially of scalp)
Surgery if causing significant neurological deficit or for cosmetic purposes.
Pathophysiology of subdural haemorrhage
Stretching and tearing of bridging cortical veins as they cross the subdural space to drain into an adjacent dural sinus.
Cause of subdural haemorrhage
High impact trauma - sudden change in velocity of head
Clinical Presentation of subdural haemorrhage
Usually unconscious
Pupillary abnormalities
May be latent (delayed presentation)
Why are young people more likely to have an extradural haemorrhage whereas older people are more likely to have a subdural haemorrhage?
Dura becomes more adherent to skull with age.
Cause of extradural haemorrhage
High impact trauma (associated with skull fracture)
Clinical presentation of extradural haemorrhage
May or may not lose consciousness transiently after trauma.
Regain consciousness but usually have an ongoing headache before losing consciousness again gradually.
Some CNIII and VI involvement.
Cause of subarachnoid haemorrhage
Spontaneous intracranial haemorrhage - ruptured aneurysm, venous infarct, cocaine use
OR traum
Risk factors for subarachnoid haemorrhage
Older middle age (50-60)
Hypertension
Alcohol consumption
Management of subarachnoid haemorrhage
ICP monitoring Prevention of cerebral vasospasm: Haemodilution - reduces haematocrit Hypertension - increase blood pressure Hypervolaemia - correction of hypovolaemia Nimodipine - Cerebral selective CCB Vasodilating agents/Balloon angioplasty
Causes of intracerebral haemorrhage
Haemorrhagic venous infarct
Hypertensive haemorrhage
Haemorrhagic transformation of ischaemic tract
Risk factors intracerebral haemorrhage
HTN Diabetes Smoking Alcohol Severe migraine Age
Clinical presentation of intracerebral haemorrhage
Headache One sided weakness Vomiting Seizures LOC Neck stiffness
Management of intracerebral haemorrhage
Stop warfarin
Control hypertension
Surgery for large superficial haematomas
Cause of intraventricular haemorrhage
Trauma Haemorrhaging in stroke Aneurysm Vascular malformation Tumors (particularly of choroid plexus)
Presentation of intraventricular haemorrhage
Headache
N+V
Altered mental state and conscious level
Xanthochromia
Management of intraventricular haemorrhage
Symptomatic treatment
Investigate cause of bleed
Treat hydrocephalus w/ EVD or ventriculoperitoneal shunt
Causes of obstructive hydrocephalus
Tumour Abscess Cysts Congenital Aqueduct Stenosis Chiari Malformations
Chiari Malformations
Downward displacement of cerebellar tonsils causing obstructive hydrocephalus
Causes of non obstructive hydrocephalus
Intracranial haemorrhage (SAH, IVH)
Infection - meningitis
Post traumatic
Management of obstructive hydrocephalus
Endoscopic Third Ventriculostomy - opening in floor of 3rd ventricle, redirecting CSF into space anterior to brainstem.
Management of non obstructive hydrocephalus
Insertion of ventriculoperitoneal shunt
Common organisms in intracranial infections
Anaerobic/aerobic streptococci
Staph Aureus
Sources of intracranial infections
Paranasal sinus infections Dental abscess Middle ear and mastoid infection Haematogenous spread Penetrating head trauma Post op
Empyema
Accumulation of pus
History and presentation of intracranial infections
Headache N+V Seizures Altered mental state Neck stiffness Focal neurological defects
May have had a previous infection which has reached CNS.
Indication for mannitol
Traumatic brain injury causing raised ICP
Route of administration of mannitol
IV
MOA of mannitol
Osmotherapeutic - draws fluid out of oedematous nerve tissue into blood osmotically
ADRs of mannitol
Electrolytes imbalance
Diuresis
Hypotension
Thrombophlebitis
Contraindications of mannitol
Anuric Intracranial bleed (blood brain barrier compromised)
Indication for dexamethasone
Traumatic brain injury
Route of administration of dexamethasone
IV
MOA of dexamethasone
Steroid - forms a complex with glucocorticoid receptor which acts as a transcriptional regulator. Upregulation of anti inflammatory proteins and down regulation of proinflammatory proteins.
ADRs of dexamethasone
Immunosuppression (long term)
Cushing’s Syndrome
Osteoporosis
Contraindications of dexamethasone
Immunocompromised
Diabetic
Indication for midazolam
Epilepstic seizure
Route of administration of midazolam
Buccal or rectal
MOA of midazolam
Benzodiazepines - increase GABAergic suppression of nerve activity. Increased Cl- in cell, hyperpolarisation and therefore reduced impulse propagation
ADRs of midazolam
Drowsiness
Cardiac arrest
Paradoxical excitement/aggression
Contraindications of midazolam
CNS depression
Severe respiratory depression
Indication for carbamazepine
Long term management of epilepsy - reduces incidence of seizures
Route of administration of carbamazepine
Oral
MOA of carbamazepine
Na+ channel blocker
GABA agonist
Therefore, reduces aberrant action potential propagation
ADRs of carbamazepine
Allergic skin reaction aplastic anaemia (damage to bone marrow and haemopoietic stem cells) Atazia Blurred vision Dizziness
Contraindications of Carbamazepine
Porphyria (build up of porphryn proteins which are essential for Hb function)
Cardiac AV blocking drugs.
Status Epilepticus
A medical emergency -
seizure lasting more than 5 minutes or 2 seizures occurring within 5 minutes
Level of bifurcation of brachiocephalic trunk
Right sternoclavicular joint
Level of bifurcation of common carotid arteries
Superior margin of thyroid cartilage C4
Coronary Sinuses
Dilatation of internal and common carotids at the carotid triangle (bifurcation) - involved in regulation of blood pressure
Internal carotid arteries supply…
Brain
Eyes
Forehead
Do not supply any structures in the neck.
Major branches of the external carotid arteries…
Maxillary - supply deep structures of the face
Facial and superficial temporal branches - supply superficial areas of the face
Vertebral arteries supply:
The brain (converge to form basilar artery)
External jugular vein
Drains external face into subclavian vein
Internal jugular vein
Drains facial, lingual, occipital, superior and middle thyroid veins.
Combines with subclavian vein to form brachiocephalic vein
Dural venous sinuses drain into…
Internal jugular vein
Cavernous Sinuses
Next to sphenoid bone.
Receive blood from ophthalmic veins, middle superficial cerebral veins and sphenoparietal sinus.
Contain internal carotid artery - cooling the blood before it reaches the brain.
Why does cavernous sinus infection cause nerve damage?
Lateral wall of each cavernous sinus contains CNIII, CNIV, CNV1 and CNV2
Contents of carotid sheath
Common and internal carotid arteries
Internal jugular vein
Vagus nerve
Deep cervical lymph nodes
Cranial nerves which exit the skull via the cribriform plate
CNI - Olfactory nerve
Cranial nerves which exit the skull via the optic canal
CNII - Optic Nerve
Cranial nerves which exit the skull via the superior orbital fissure
CNIII - Oculomotor nerve
CNIV - Trochlear nerve
CNV1 - Ophthalmic branch of Trigeminal Nerve
CNVI - Abducens Nerve
Cranial nerves which exit the skull via the internal auditory canal
CNVII - Facial Nerve
CNVIII - Vestibulocochlear Nerve
Cranial nerves which exit the skull via the jugular foramen
CNIX - Glossopharyngeal nerve
CNX - Vagus Nerve
CNXI - Accessory Nerve
Cranial nerves which exit the skull via the hypoglossal canal
CNXII - Hypoglossal Nerve
Function of nasal cavity
Warms and humidifies inspired air
Removes and traps pathogens and particulate matter from inspired air
Sense of smell
Drainage and clearance of paranasal sinuses and lacrimal ducts
Epithelium found in the nasal cavity
Respiratory region (majority) - ciliated pseudostratified epithelium, interspersed with mucus secreting goblet cells. Olfactory region (upper apex) - olfactory cells with olfactory receptors
Function of nasal conchae
Increased surface area of nasal cavity, making airflow slow and turbulent.
Therefore, air remains in cavity longer for humidification
Structures which open into nasal cavity
Sphenoid, ethmoidal, maxillary, frontal sinuses
Eustachian tube
Nasolacrimal duct
Ethmoid Bulla
Opening of middle ethmoid sinus into nasal cavity
Arterial supply to nasal cavity
Internal and external carotid arteries
Venous drainage of nasal cavity
Pterygoid plexus
Facial vein
Cavernous sinus
Kiesselbach Area
Anterior 1/3 of nasal cavity, common site of epistaxis (nosebleed) due to rich blood supply.
Innervation of nose and nasal cavity
Specifal sensation via olfactory nerves and olfactory bulb
General sensation to septum and lateral walls via nasopalatine (CNV2)and nasociliary (CNV1) nerve.
CNV supplies external skin of nose.
Significant risk associated with Cribriform plate fracture
CNS infection (meningitis, encephalitis, brain abscesses) since fractured cribriform plate can penetrate meningeal linings causing leakage of CSF.
Anosmia
Loss of smell
Can occur due to damage of olfactory bulb in cribriform plate fracture.
Vertebral level of larynx
C3-6
Glottis of larynx contains
Vocal cords
Interior surface of larynx is lined by…
Mucus membrane containing ciliated columnar epithelium
Blood supply to larynx
Superior laryngeal artery (from superior thyroid)
Inferior laryngeal artery (from inferior thyroid)
Function of true focal cords (Vocal laryngeal folds)
Control pitch of sound generated
Reinke’s space
Found in vocal laryngeal folds. Contains fluid and GAGs which vibrate to create sound.
Vestibular Laryngeal Folds
False vocal cords
Act to provide protection to larynx
Consist of vestibular ligament covered by a mucous membrane
Action of suprahyoid muscles
Elevate larynx
Action of infrahyoid muscles
Depress larynx
Action of cricothyroid
Stretches and tenses vocal ligament - forceful speech
Action of thyroarytenoid
Relaxes vocal ligaments - softer voice
Muscles which alter size of rima glottidis
Posterior cricoarytenoid - abducts vocal folds, widening rima glottidis
Lateral cricoarytenoid - adducts vocal folds, narrowing rima glottidis
Transverse and oblique arytenoids - adduct arytenoid cartilages, closing posterior portion of rima glottidis
Function of rima glottidis
Phonation - when air is forced through a closed RG, sound is generated.
Tracheotomy
Half inch, horizontal incision in the indentation between Adam’s Apple and the cricoid cartilage. Rought 0.5-1 inch deep.
To relieve an obstruction to breathing.
Indication for tracheotomy
Person has a throat obstruction and is not able to breath at all (not coughing or gasping) and Heimlich Maneuvre has been attempted 3 times.
Tracheostomy
An opening at the front of the neck so that a tube can be inserted into the windpipe - helping a person to breath.
Origin of sternocleidomastoid
Sternum and clavicle
Insertion of sternocleidomastoid
Mastoid process of temporal bone of the skull
Function of sternocleidomastoid
Rotation of head and flexion of the neck
Innervation of sternocleidomastoid
CNXI
Complications of interscalene bloc
Temporary paresis of thoracic diaphragm (since phrenic nerve lies in this area)
Difficulty swallowing
Vocal cord paresis
What is interscalene block?
Injection of local anaesthetic into nerves of brachial plexus (between anterior and middle scalene muscles, at level of cricoid cartilage)
Useful for surgery of clavicle, shoulder and arm.
Suboccipital muscles
Rectus capitis posterior minor and major
Obliquus capitis superior and inferior
Actions of suboccipital muscles
Extension and rotation of head
Structures found in the suboccipital triangle
Vertebral artery
Suboccipital venous plexus
Suboccipital nerve
Action of stylohyoid muscle
Initiates swallowing by pulling hyoid postero-superiorly
Innervation of stylohyoid
Stylohyoid branch of CNVII
Action of digastric muscle
Depresses mandible and elevates hyoid bone
Innervation of digastric muscle
Anterior belly - CNV
Posterior belly - CNVII
Action of suprahyoid muscles
Elevate hyoid bone
Scalene muscles:
Action:
Supplied by…
Anterior, middle and posterior
Accessory muscles of respiration AND ipsilateral flexion of neck
Supplied by anterior rami of cervical spine (A=C5-6, M=C3-8 and P=C6-8)
Jefferson Fracture
Fracture of atlas - usually caused by diving into shallow water.
Unlikely to damage spinal cord at C1 level since vertebral foramen is large (but may be damaged further down)
What type of cervical spine injury will result in spinal cord injury?
Dislocation or subluxation - 50% of cases occur at C6/7
Hangman’s Fracture
Fracture of Pars articularis of axis (C2) due to rapid deceleration
Significant risk of Dens Fracture
Unstable, at risk of avascular necrosis due to isolation of distal fragment from any blood supply.
Bones which form the superficial border of the orbit
Frontal
Zygomatic
Maxillary
Bones of the calvarium (vault of the skull)
Frontal
Parietal
Occipital
Bones of the cranial base
Frontal Ethmoid Sphenoid Temporal Parietal Occipital
Bregma
Anatomical point on the skull at which the coronal suture is intersected perpendicularly by the sagittal suture.
(Anteriosuperior)
Lambda
Anatomical point on the skull at which the lumbdoid suture is intersected perpendicularly by the sagittal suture.
(Posterior)
Arterial, Venous and nervous supply of dura mater
Middle meningeal artery and vein
CNV (trigeminal nerve)
Arterial, Venous and nervous supply of arachnoid mater
Avascular
No innervation
Arachnoid granulations
Projections of arachnoid mater into the dura which allow CSF to reenter circulation via dural venous sinuses
