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Year 2 > Case 16 > Flashcards

Case 16 Flashcards

1
Q

Uncal herniation is caused by…

A

Raised intracranial pressure

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2
Q

Uncal herniation

A

Uncus (medial edge of temporal lobe) forced below tentorium cerebelli to compress the midbrain.

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3
Q

Signs of uncal herniation

A

Abnormal posture
Poor GCS
Eye down and out, enlarged ipsilateral pupil and absent light reflex (compression of CNIII)
Potential coma (compression of midbrain)

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4
Q

Central/Trans Tentorial Herniation

A

Entire brain moving downward.
Can see symmetric downward movement of thalamic structures.
Compression of upper midbrain, therefore affecting pons and medulla as well.

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5
Q

Signs of Central/Trans Tentorial Herniation

A

Diabetes insipidus (compression of pituitary stalk)
Dilated fixed pupils.
Paralysis of upper eye movement (AKA sunset eyes)
False localising sign.

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6
Q

Most common brain herniation

A

Cingulate/Subfalcine/Transfalcine

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7
Q

Cingulate/Subfalcine/Transfalcine Herniation

A

Displacement of brain (typically cingulate gyrus) under falx cerebri, across midline

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8
Q

Signs of Cingulate/Subfalcine/Transfalcine Herniation

A

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)

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9
Q

Foramen of Monroe

A

Interventricular foramen between lateral ventricles and 3rd ventricle.

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10
Q

Foraminal/Tonsillar Herniation

A

Downward herniation of cerebellar tonsils into foramen magnum.

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11
Q

Signs of Foraminal/Tonsillar Herniation

A

Respiratory arrest (compression of respiratory centre in medulla)

Instant deterioration

No other signs since structures superior to medulla are unaffected.

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12
Q

Vertebral arteries arise from…

A

Subclavian arteries

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13
Q

Vertebral arteries fuse to form…

A

Basilar artery

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14
Q

Blood supply to brainstem

A

Vertebral and basilar arteries.

Therefore, strokes involving these arteries have a high mortality (85%) since brainstem controls life support functions.

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15
Q

Ascending Reticular Activating System (ASAS) controls…

A

Consciousness

Consists of many components in brainstem - damage results in coma.

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16
Q

Signs/Symptoms of damage to spinothalamic tract

A

Contralateral loss of pain and temperature sensation on the body

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17
Q

Signs/Symptoms of damage to trigeminal tract

A

Ipsilateral loss of pain/temperature sensation on the face

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18
Q

Nucleus Ambiguus

A

Located in medullary reticular activating system.

Innervation of muscles of soft palate, pharynx and larynx

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19
Q

Signs/Symptoms of damage to Nucleus Ambiguus and Nerve roots of CNIX and X

A

Dysphagia
Hoarseness
Loss of gag reflex

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20
Q

Lateral medullary syndrome is caused by

A

Occlusion of Posterior Inferior Cerebellar Artery

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21
Q

Signs/Symptoms of damage to Hypothalamospinal Fibres (Dorsal Longitudinal Fasciculus

A

Ipsilateral Horner’s Syndrome

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22
Q

Signs/Symptoms of damage to Vestibular Nuclei

A

Vetigo
Tendency to fall to ipsilateral side
Diplopia (double vision)

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23
Q

Signs/Symptoms of damage to spinocerebellar tract

A

Ipsilateral ataxia

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24
Q

Cause of lateral medullary syndrome

A

PICA occlusion

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25
Q

PICA

A

Posterior Inferior Cerebellar Artery

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26
Q

Signs/Symptoms of Lateral Medullary Syndrome

A

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

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27
Q

Spinal tracts affected by lateral medullary syndrome

A 
Spinothalamic tract 
Trigeminal Tract 
Nucleus Ambiguus and roots of CNIX and X
Hypothalamospinal Fibres 
Vestibular Nuclei 
Spinocerebellar Tract
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28
Q

Glial cell division occurs…

A

Throughout life

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29
Q

Neuronal cell division occurs…

A

Before birth

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30
Q

Brain cells found in brain tumors

A

Glial cells (glioma)
OR
Cells of meningeal coverings (Meningioma)

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31
Q

Function of Microglia

A

Attack disease organisms and phagocytose damaged cells

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32
Q

Function of oligodendrocytes

A

Myelination

Schwann cells of the CNS.

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33
Q

Necrosis

A

Loss of membrane integrity, resulting in release of inflammatory mediators which can cause further damage.

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34
Q

Apoptosis

A

Programmed cell death.
Cell breaks up into membrane bound bodies containing intact organelles.
No release of inflammatory mediators.

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35
Q

Cellular changes resulting in apoptosis

A

Loss of trophic factors needed for cell survival - BDNF and NGF.
Extracellular ligands e.g. TNF

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36
Q

Apoptosis is orchestrated by…

A

Proteolytic enzymes called caspases

DNAases

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37
Q

Galectin-1

A

Factor secreted by macrophages that promotes Schwann Cell migration and axon regrowth following axonal injury.

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38
Q

Function of Schwann cells in axonal regeneration

A

Phagocytose debris

Secrete trophic factors to promote axonal growth.

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39
Q

Function of Calpain in axonal regeneration

A

Breakdown of cytoskeleton

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40
Q

Function of macrophages in axonal regeneration

A

Secrete factors (e.g. Galectin-1) that promote axon regrowth and schwann cell migration

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41
Q

Function of microglia in Glial Scar formation

A

Removal of debris

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42
Q

Function of Astrocytes in Glial Scar Formation

A

Begin to divide and hypertrophy 48 hrs after injury.

Reform a barrier to the brain by linking of their processes together around the lesion.

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43
Q

Function of Meningeal-like cells in Glial Scar Formation

A

Invade the lesion cavity to form a plug

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44
Q

Cytokines involved in Glial Scar formation…

Released by…

A

IL-6, TGF-beta, FGF-2

Microglia, neurons and astrocytes

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45
Q

Key cell in Glial Scar Formation

A

Astrocytes

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46
Q

Why does axonal regrowth not occur in CNS?

A

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)

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47
Q

Diffuse axonal injury

A

A shearing injury causing extensive lesions in white matter tracts occurring over a widespread area.

Results in immediate unconsciousness

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48
Q

Why does unconsciousness occur?

A

Functional disturbance in Ascending Reticular Activating system (responsible for consciousness and arousal)

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49
Q

Protein associated with DAI

A

Beta-amyloid protein, accumulates 2-3 hours post injury

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50
Q

Petechial Haemorrhages in the brain

A

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)

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51
Q

White matter haemorrhage due to DAI can result in…

A

Complete loss of corpus callosum and enlargement of ventricles.

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52
Q

Function of Nerve Growth Factor and Brain-Derived Neurotrophic Factor

A

Released at synapses. Maintain and promote survival of neurons.

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53
Q

Transneuronal Degeneration

A

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.

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54
Q

Why does extracellular [Glutamate] rise in traumatic brain injury?

A

Rupture of axons causing release of glutamate.

Anaerobic metabolism by astrocytes resulting in acidity and therefore, reduced reuptake of glutamate.

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55
Q

Cellular Consequences of Excitotoxicity

A

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

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56
Q

Molecules responsible for prevention of oxidative stress

A

Reactive oxygen species produced in oxidative phosphorylation by mitochondria.
Mopped up by vitamins A and E, superoxide dismutase, catalase and glutathione peroxidase.

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57
Q

Why does excitotoxicity result in oxidative stress?

A

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

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58
Q

Symptoms of Meningitis

A

Headache, fever, stiffness (TRIAD)

+

Photophobia
Altered consciousness
Seizures
Non blanching rash

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59
Q

Signs of Bacterial Meningitis

A

Headache, fever and neck stiffness (TRIAD)

Altered consciousness, low blood pressure, petechial rash, tachycardia.

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60
Q

How does viral meningitis differ from bacterial meningitis clinically?

A

Viral is less severe, often self-limiting.

Viral causes high fever but BP remains normal and there is no rash.

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61
Q

Causes of RBCs in CSF

A

Traumatic Tap

Intrathecal bleeding

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62
Q

How do you distinguish between traumatic tap and intrathecal bleeding in CSF examination?

A

Traumatic tap - RBC count will decrease in number across multiple samples.

Intrathecal bleeding - RBC count is consistent across multiple samples.

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63
Q

Xanthochromia

A

Yellow tinge in CSF samples after blood products have been present for 12hrs

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64
Q

> 90% polymorphs (neutrophils in CSF

A

Bacterial infection

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65
Q

> 90% lymphocytes in CSF

A

Viral infection

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66
Q

Normal white cell count in CSF

A

No white cells is NORMAL.

<5 is acceptable unless there is sufficient history

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67
Q

CSF in bacterial meningitis

A

Yellowish, turbid
Increased polymorphs
Increased proteins
Decreased glucose

Normal lymphocytes

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68
Q

CSF in viral meningitis

A

Clear fluid
Increased lymphocytes

Normal lymphocytes, protein and glucose

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69
Q

Bacterial causes of meningitis

A 
Neisseria Meningitidis (Gram -ve)
Streptococcal pneumoniae (Gram +ve)
Listeria Monocytogenes (Gram +ve)
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70
Q

Viral cause of meningitis

A

Enterovirus

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71
Q

Treatment of bacterial meningitis

A

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

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72
Q

Treatment for viral meningitis

A

Analgesia
Antiemetics
Hydration

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73
Q

When is a CT scan of head indicated in meningitis?

A

Raised ICP
Immunocompromised
Reduced GCS

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74
Q

Chronic Meningitis

A

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

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75
Q

CSF in fungal meningitis

A

Yellow and viscous
Increase lymphocytes
Protein and polymorphs may be increased or normal
Glucose may be decreased or normal.

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76
Q

Symptoms of encephalitis

A

Headache
Seizure
Personality change
Neurological signs

(May first present in psychiatric services)

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77
Q

Causes of encephalitis

A 
Herpes Simplex 
CMV
EBV
Varicella Zoster 
HIV
Enterovirus 
Measles Virus

Can also be autoimmune

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78
Q

Treatment of viral encephalitis

A

Aciclovir

or HAART if secondary to HIV/AIDS

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79
Q

MOA of Aciclovir

A

DNA polymerase inhibitor.

Inhibits DNA synthesis by virus.

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80
Q

Karposi Sarcoma

A

Tumour caused by Human Herpes Virus 8 - lesions in skin, mucus membranes and lymph nodes due to poor control of HIV

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81
Q

Vacuolar Myelopathy

A

Associated with low CD4+ lymphocytes in HIV.

Symptoms include:
Painless leg weakness, stiffness, sensory loss, imbalance, sphincter dysfunction

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82
Q

Paralytic Poliomyelitis

A

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.

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83
Q

Cause of intracerebral abscess/empyema

A

Local infection (e.g. mastoid air cells, venous sinuses, otitis media) that spreads intracranially

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84
Q

Symptoms of rabies

A 
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

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85
Q

Virus which causes rabies

A

Lyssavirus

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86
Q

Negri bodies

A

Eosinophilic, sharply outlined bodies found in cytoplasm of neurons infected with lyssavirus (rabies). Especially pyramidal cells within Ammon’s horn of the hippocampus.

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87
Q

Treatment of rabies

A

Hospitalisation
Immunoglobulin treatment
Anti-rabies vaccine

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88
Q

Symptoms of tetanus

A

Spasms and stiffness in jaw muscles (trismus/lock jaw)
Stiffness of neck and abdominal muscles
Difficulty swallowing
Painful body spasms (last several minutes)

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89
Q

How does Botulinism manifest in the body?

A

Clostridium botulinism is a bacteria found in soil and canned foods.
Secretes botulinum toxin (botox) which causes symptoms of botulinism when ingested.

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90
Q

Signs/Symptoms of Botulinism

A 
Descending paralysis including respiraory failure.
Blurred vision
Pupil dilatation 
Nausea 
Diarrhoea
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91
Q

Treatment of botulinism

A

Intubation

Antitoxin

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92
Q

Most common parasitic disease of CNS

A

Taenia Solium - cysticercosis

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93
Q

Most common cause of epilepsy worldwide

A

Cysticercosis - Taenia Solium parasite infection

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94
Q

Signs/Symptoms of Cysticercosis

A

New onset of seizures +/- raised ICP if CSF flow is interrupted

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95
Q

Treatment of cysticercosis/Taenia Solium

A

Praziquantel or Albendazole - used n treatment of parasitic worm infections

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96
Q

Bacteria responsible for neurosyphilis

A

Treponema Pallidum

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97
Q

Manifestations of Tertiary Syphilis

A

Neurosyphilis
Gumma
Aortitis/Aortic regurgitation

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98
Q

Latency of neurosyphilis

A

Pure meningeal = 1yr
Meningovascular = 5-10yrs
Spinal cord involvement =20yrs

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99
Q

Treatment of syphilis

A

Penicillin

Probenicid

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100
Q

Prion disease of CNS

A

85% caused by Sporadic Creutzfeldt-Jakob

Brain damage leading to rapid decrease of movement and mental function.

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101
Q

Signs and symptoms of Prion Disease of CNS

A 
Neurodegenerative:
Dementia
Seizures
Personality change
Ataxia 
Startle myoclonus (sudden muscle contraction)
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102
Q

Metabolic causes of coma without neurological signs

A 
Hyper/Hypoglycaemia 
Hypoxia
Acidosis 
Thiamine Deficiency
Hepatic or Renal Failure 
Hypercapnia 
Hypoadrenalism
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103
Q

Most common category of coma

A

Coma without neurological signs

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104
Q

Toxins resulting in Toxin-Induced Coma without neurological signs

A

Drugs - benzodiazepines, Barbiturates, opiates, TCAs

Alcohol

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105
Q

Non metabolic, non toxic causes of Coma without neurological signs

A

Infectious e.g. encephalitis
Vascular e.g. hypertensive encephalopathy
Trauma e.g. concussion
Epilepsy (postictal - after a seizure)
Temperature regulation i.e. hypo/hyperthermia

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106
Q

Causes of coma with neurological signs

A

Haemorrhage
Infarction
Tumours
Infectious (abscess)

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107
Q

Causes of coma in meningitic syndrome

A

Subarachnoid haemorrhage

Bacterial meningeal infection

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108
Q

Tentorium

A

Outgrowth of dura mater, separating cerebellum and cerebrum

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109
Q

Components of reticular formation

A

Diencephalon (consists of thalamus, hypothalamus and pituitary gland, effectively enclosing the 3rd ventricle)
Midbrain
Rostral pons

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110
Q

Components of reticular activating system

A

Reticular formation
Thalamus
Cerebral hemispheres

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111
Q

Symptoms of raised ICP

A 
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

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112
Q

False localising sign in raised ICP

A

CNVI compression - signs do not indicate location of the problem.

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113
Q

Cheyne-Stokes Respiration

A

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.

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114
Q

Kussmaul Respiration

A

Deep and laboured breathing associated with metabolic acidosis (e.g. DKA)

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115
Q

Apneusis

A

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)

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116
Q

Ataxic breathing

A

Complete irregularity of breathing.

Caused by damage to medulla oblongata.

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117
Q

Apneustic centre

A

Located in pons

Controls rhythm of breathing

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118
Q

Pneumotactic centre

A

Located in pons
Controls rate and depth of breathing
Inhibits apneustic centre

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119
Q

GCS: Best eye opening response

A

Spontaneously 4
To verbal stimuli 3
To painful stimuli 2
None 1

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120
Q

GCS: Best Verbal response

A 
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible 2
No verbal response 1
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121
Q

Best motor response

A 
Obeys commands 6
Localises pain 5
Withdraws to pain 4
Flexion to pain 3
Extension to pain 2
None 1
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122
Q

Divergence of eyes in the unconscious patient

A

Normal during drowsiness,

Ocular axes become parallel as coma deepens i.e. drift back to middle.

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123
Q

Conjugate Roving

A

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

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124
Q

Ocular bobbing

A

Brisk downward movement of eyes, slow movement back up to primary position.
Caused by damage to PONS bilaterally

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125
Q

Small, reactive pupils in the unconscious patient

A

Damage to diencephalon (thalamus, hypothalamus and 3rd ventricle)

Drugs

Metabolic encephalopathy

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126
Q

Large, fixed pupils in the unconscious patient

May show hippus (spastic contraction)

A

Pretectum area of midbrain damaged

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127
Q

Pretectum of midbrain is responsible for…

A

Constriction of pupil

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128
Q

In the unconscious patient, one eye has a normal pupil, the other is dilated and fixed.

A

CN III compression

e.g. Uncal Herniation

129
Q

In an unconscious patient, pupils are in the midposition and fixed size

A

Midbrain damaged

130
Q

In an unconscious patient, pupils are very small (pinpoint)

A

Pons damaged

131
Q

In what order are eye reflexes lost in the unconscious patient

A

First, reflex eye movements
Second, corneal reflex
Third, pupillary reflex to light

132
Q

Vestibulo-ocular reflex

A

When head rotates to one side, the eyes move to the other

133
Q

Vestibulo-ocular reflex assesses function of…

A

Medial longitudinal fasciculus in brainstem - main centre of connection for CN III, IV and VI

134
Q

When turning the head of an unconscious patient (Doll’s eye manoeuvre), the eyes move to the ipsilateral side. Area of damage is?

A

Medial longitudinal fasciculus in brainstem

135
Q

Normal result in caloric testing

A

Eyes deviate to side of unpleasant stimulus AND nystagmus

136
Q

Caloric testing

A

Irrigation of one ear with 20ml of cold water. Eye movements are assessed.

137
Q

On carrying out a caloric test on an unconscious patient, there is no nystagmus in both eyes. This indicates…

A

Low brainstem lesion

138
Q

On carrying out a caloric test on an unconscious patient, there is no nystagmus in one eye. This indicates…

A

Medial Longitudinal Fasciculus lesion

139
Q

Unconscious patient with hypertonia

A

Established (long term) damage to cortex or proximal cervical spine.

140
Q

Unconscious patient with flaccid paralysis

A

Acute spinal cord injury

Hypertonia develops over time

141
Q

Decorticate posturing of unconscious patient

A

Arms adducted, flexed at the elbow and wrist.

Caused by damage to one or both corticospinal tracts

142
Q

Decerebrate posturing of unconscious patient

A

Arms adducted, extended at the elbow, pronated and flexed at the wrist.

Caused by damage to upper brainstem

143
Q

Precentral gyrus contains

A

Primary motor cortex

144
Q

Arrangement of primary motor cortex

A

Leg closest to midline.

Face most lateral

145
Q

PMC is found in which lobe?

A

Frontal lobe

146
Q

Broca’s Area

A

Motor speech centre in frontal lobe

147
Q

Arrangement of primary sensory cortex

A

Leg closest to midline.

Face most lateral

148
Q

Occipital lobe contains

A

Visual cortex

149
Q

Temporal Lobe functions

A 
Contains primary auditory cortex - involved in hearing.
Involved in formation of new memories and interpretation of visual stimuli
Language comprehension (contains Wernicke's Area)
150
Q

Location of insular lobe

A

Deep to lateral surface of brain (underneath frontal, parietal and temperal lobes.

151
Q

Function of insula

A 
Primary gustatory cortex 
language 
visual-vestibular integration 
Sympathetic tone 
Perception, motor control, self awareness and cognitive functioning
152
Q

Damage to insula is associated with

A

arrhythmias

153
Q

Basal ganglia

A

Lentiform nucleus (Globus pallidus and Putamen)
Caudate nucleus
Substantia nigra
Subthalamic nuclei

154
Q

Function of lentiform nuclei

A

Regulation of movement

155
Q

Function of caudate nucleus

A

Memory and learning

156
Q

Corpus striatum consists of…

A 
Lentiform nucleus (Globus pallidus and Putamen)
Caudate nucleus
157
Q

Function of thalamus

A

Relay of sensory information to cortex.

Sleep, wakefulness, consciousness and arousal.

158
Q

Thalamus is supplied by…

A

Posterior cerebral artery

159
Q

Corona Radiata in the brain

A

White matter tract which is an extension of internal capsule, carrying ascending and descending fibres.

160
Q

Most common sites of intracranial aneurysm

A 
Anterior communicating (40%)
Bifurcation of middle cerebral (34%)
Posterior communicating (20%)
Basilar Tip (4%)
161
Q

Arterial supply of Caudate nucleus

A

Anterior cerebral artery

162
Q

Arterial supply of Lentiform nucleus

A

Middle cerebral artery

163
Q

Arterial supply of thalamus

A

Posterior cerebral artery

164
Q

Arterial supply of internal capsule

A

Anterior choroidal artery

165
Q

Torcular Herophili

A

Confluence of sinuses of the cerebrum

166
Q

Venous sinuses of cerebrum drain into…

A

Internal jugular vein

167
Q

Foramen of Monro

A

Connects lateral ventricles to the 3rd ventricle

168
Q

Sylvian Aqueduct

A

Connects 3rd and 4th ventricle

169
Q

Foramen of Luschka

A

Links 4th ventricle to cerebellopontine cistern. Allows CSF to enter subarachnoid space.

170
Q

Foramen of Magendie

A

Links 4th ventricle and foramen magnum. Allows CSF to enter subarachnoid space.

171
Q

Lobes of cerebellum

A

Anterior (petrosal)
Superior (tentorial)
Inferior (suboccipital)

172
Q

Function of cerebellum

A

Coordination and timing of movements

173
Q

Where is the cerebellum situated?

A

Posterior cranial fossa, behind 4th ventricle, pons and medulla.

174
Q

Tentorium cerebelli

A

Separates cerebellum from cerebrum

175
Q

Components of midbrain

A

Tectum
Tegmentum
Cerebral peduncles (containing ascending and descending tracts to and from cerebrum)

176
Q

Arterial supply of pons

A

Superior cerebellar artery

Pontine branches of basilar artery

177
Q

Ventral pons contains

A

White matter tracts: Corticospinal and corticobulbar

178
Q

Which cranial nerves arise from Dorsal Tegmentum of Pons?

A

CNV, VI, VII and VIII

179
Q

Mesencephalon

A

Midbrain

180
Q

Metencephalon

A

Pons

181
Q

Myencephalon

A

Medulla Oblongata

182
Q

Corticobulbar tract

A

Supplies muscles of head and neck

183
Q

Bulbar reflexes

A

Coughing, sneezing, swallowing and vomiting

184
Q

Medulla Oblongata contains…

A

Autonomic cardiovascular and respiratory centres - controls breathing, blood pressure and heart rate

Reflex centres for bulbar reflexes e.g. vomiting and sneezing

185
Q

Arterial supply to medulla oblongata

A

PICA
Anterior spinal artery
Vertebral arteries

186
Q

Ventral/Anterior medulla oblongata contains…

A

Olive
Pyramidal tracts (e.g. corticospinal)
CN IX-XII rootlets

187
Q

Tegmentum/Dorsal medulla oblongata contains…

A

CN nuclei

White matter tracts

188
Q

Decussation of pyramids occurs in the…

A

Medulla oblongata

189
Q

Prevertebral soft tissue spaces seen on a lateral C-Spine X-Ray

A

C1 Nasopharyngeal
C2-4 Retropharyngeal
C5-7 Retrotracheal

190
Q

Normal size for C1 Nasopharyngeal space on a lateral C-Spine X-Ray

A

<10mm

191
Q

Normal size for C2-4 Retropharyngeal space on a lateral C-Spine X-Ray

A

<5-7mm

192
Q

Normal size for C5-7 Retrotracheal space on a lateral C-Spine X-Ray

A

<22mm (or <14mm in children)

193
Q

Mechanism for Hangman’s Fracture

A

Hyperextension (e.g. hanging, chin hitting dashboard in car accident)

194
Q

What is a Hangman’s Fracture?

A

Fracture through pedicle of the axis

195
Q

Radiographic features of a Hangman’s Fracture

A

Prevertebral swelling
Anterior dislocation of the C2 vertebral body
Bilateral C2 pedicle fractures

196
Q

Radiographic features of bilateral facet dislocation

A

Complete anterior dislocation of affected body by half or more of the vertebral body AP diameter

197
Q

Management of brain contusion

A

Observe for signs of raised ICP (craniotomy/ectomy for persistently raised ICP)
Prevent hypoxia and hypotension

198
Q

Craniectomy

A

Removal of part of skull to allow a swelling brain to expand

199
Q

Craniotomy

A

Surgical removal of part of skull to expose part of brain

200
Q

Cause of depressed skull fracture

A

Impact with a sharp edge e.g. brick, hammer

201
Q

Management of depressed skull fracture

A

Usually conservative
Clean and suture overlying lacerations (especially of scalp)
Surgery if causing significant neurological deficit or for cosmetic purposes.

202
Q

Pathophysiology of subdural haemorrhage

A

Stretching and tearing of bridging cortical veins as they cross the subdural space to drain into an adjacent dural sinus.

203
Q

Cause of subdural haemorrhage

A

High impact trauma - sudden change in velocity of head

204
Q

Clinical Presentation of subdural haemorrhage

A

Usually unconscious

Pupillary abnormalities

May be latent (delayed presentation)

205
Q

Why are young people more likely to have an extradural haemorrhage whereas older people are more likely to have a subdural haemorrhage?

A

Dura becomes more adherent to skull with age.

206
Q

Cause of extradural haemorrhage

A

High impact trauma (associated with skull fracture)

207
Q

Clinical presentation of extradural haemorrhage

A

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.

208
Q

Cause of subarachnoid haemorrhage

A

Spontaneous intracranial haemorrhage - ruptured aneurysm, venous infarct, cocaine use

OR traum

209
Q

Risk factors for subarachnoid haemorrhage

A

Older middle age (50-60)
Hypertension
Alcohol consumption

210
Q

Management of subarachnoid haemorrhage

A 
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
211
Q

Causes of intracerebral haemorrhage

A

Haemorrhagic venous infarct
Hypertensive haemorrhage
Haemorrhagic transformation of ischaemic tract

212
Q

Risk factors intracerebral haemorrhage

A 
HTN
Diabetes 
Smoking 
Alcohol
Severe migraine 
Age
213
Q

Clinical presentation of intracerebral haemorrhage

A 
Headache 
One sided weakness 
Vomiting 
Seizures 
LOC 
Neck stiffness
214
Q

Management of intracerebral haemorrhage

A

Stop warfarin
Control hypertension
Surgery for large superficial haematomas

215
Q

Cause of intraventricular haemorrhage

A 
Trauma 
Haemorrhaging in stroke 
Aneurysm 
Vascular malformation 
Tumors (particularly of choroid plexus)
216
Q

Presentation of intraventricular haemorrhage

A

Headache
N+V
Altered mental state and conscious level
Xanthochromia

217
Q

Management of intraventricular haemorrhage

A

Symptomatic treatment
Investigate cause of bleed
Treat hydrocephalus w/ EVD or ventriculoperitoneal shunt

218
Q

Causes of obstructive hydrocephalus

A 
Tumour 
Abscess
Cysts 
Congenital Aqueduct Stenosis 
Chiari Malformations
219
Q

Chiari Malformations

A

Downward displacement of cerebellar tonsils causing obstructive hydrocephalus

220
Q

Causes of non obstructive hydrocephalus

A

Intracranial haemorrhage (SAH, IVH)
Infection - meningitis
Post traumatic

221
Q

Management of obstructive hydrocephalus

A

Endoscopic Third Ventriculostomy - opening in floor of 3rd ventricle, redirecting CSF into space anterior to brainstem.

222
Q

Management of non obstructive hydrocephalus

A

Insertion of ventriculoperitoneal shunt

223
Q

Common organisms in intracranial infections

A

Anaerobic/aerobic streptococci

Staph Aureus

224
Q

Sources of intracranial infections

A 
Paranasal sinus infections 
Dental abscess
Middle ear and mastoid infection 
Haematogenous spread 
Penetrating head trauma 
Post op
225
Q

Empyema

A

Accumulation of pus

226
Q

History and presentation of intracranial infections

A 
Headache
N+V
Seizures
Altered mental state 
Neck stiffness
Focal neurological defects

May have had a previous infection which has reached CNS.

227
Q

Indication for mannitol

A

Traumatic brain injury causing raised ICP

228
Q

Route of administration of mannitol

A

IV

229
Q

MOA of mannitol

A

Osmotherapeutic - draws fluid out of oedematous nerve tissue into blood osmotically

230
Q

ADRs of mannitol

A

Electrolytes imbalance
Diuresis
Hypotension
Thrombophlebitis

231
Q

Contraindications of mannitol

A 
Anuric 
Intracranial bleed (blood brain barrier compromised)
232
Q

Indication for dexamethasone

A

Traumatic brain injury

233
Q

Route of administration of dexamethasone

A

IV

234
Q

MOA of dexamethasone

A

Steroid - forms a complex with glucocorticoid receptor which acts as a transcriptional regulator. Upregulation of anti inflammatory proteins and down regulation of proinflammatory proteins.

235
Q

ADRs of dexamethasone

A

Immunosuppression (long term)
Cushing’s Syndrome
Osteoporosis

236
Q

Contraindications of dexamethasone

A

Immunocompromised

Diabetic

237
Q

Indication for midazolam

A

Epilepstic seizure

238
Q

Route of administration of midazolam

A

Buccal or rectal

239
Q

MOA of midazolam

A

Benzodiazepines - increase GABAergic suppression of nerve activity. Increased Cl- in cell, hyperpolarisation and therefore reduced impulse propagation

240
Q

ADRs of midazolam

A

Drowsiness
Cardiac arrest
Paradoxical excitement/aggression

241
Q

Contraindications of midazolam

A

CNS depression

Severe respiratory depression

242
Q

Indication for carbamazepine

A

Long term management of epilepsy - reduces incidence of seizures

243
Q

Route of administration of carbamazepine

A

Oral

244
Q

MOA of carbamazepine

A

Na+ channel blocker
GABA agonist

Therefore, reduces aberrant action potential propagation

245
Q

ADRs of carbamazepine

A 
Allergic skin reaction
aplastic anaemia (damage to bone marrow and haemopoietic stem cells)
Atazia 
Blurred vision
Dizziness
246
Q

Contraindications of Carbamazepine

A

Porphyria (build up of porphryn proteins which are essential for Hb function)
Cardiac AV blocking drugs.

247
Q

Status Epilepticus

A

A medical emergency -

seizure lasting more than 5 minutes or 2 seizures occurring within 5 minutes

248
Q

Level of bifurcation of brachiocephalic trunk

A

Right sternoclavicular joint

249
Q

Level of bifurcation of common carotid arteries

A

Superior margin of thyroid cartilage C4

250
Q

Coronary Sinuses

A

Dilatation of internal and common carotids at the carotid triangle (bifurcation) - involved in regulation of blood pressure

251
Q

Internal carotid arteries supply…

A

Brain
Eyes
Forehead

Do not supply any structures in the neck.

252
Q

Major branches of the external carotid arteries…

A

Maxillary - supply deep structures of the face

Facial and superficial temporal branches - supply superficial areas of the face

253
Q

Vertebral arteries supply:

A

The brain (converge to form basilar artery)

254
Q

External jugular vein

A

Drains external face into subclavian vein

255
Q

Internal jugular vein

A

Drains facial, lingual, occipital, superior and middle thyroid veins.
Combines with subclavian vein to form brachiocephalic vein

256
Q

Dural venous sinuses drain into…

A

Internal jugular vein

257
Q

Cavernous Sinuses

A

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.

258
Q

Why does cavernous sinus infection cause nerve damage?

A

Lateral wall of each cavernous sinus contains CNIII, CNIV, CNV1 and CNV2

259
Q

Contents of carotid sheath

A

Common and internal carotid arteries
Internal jugular vein
Vagus nerve
Deep cervical lymph nodes

260
Q

Cranial nerves which exit the skull via the cribriform plate

A

CNI - Olfactory nerve

261
Q

Cranial nerves which exit the skull via the optic canal

A

CNII - Optic Nerve

262
Q

Cranial nerves which exit the skull via the superior orbital fissure

A

CNIII - Oculomotor nerve
CNIV - Trochlear nerve
CNV1 - Ophthalmic branch of Trigeminal Nerve
CNVI - Abducens Nerve

263
Q

Cranial nerves which exit the skull via the internal auditory canal

A

CNVII - Facial Nerve

CNVIII - Vestibulocochlear Nerve

264
Q

Cranial nerves which exit the skull via the jugular foramen

A

CNIX - Glossopharyngeal nerve
CNX - Vagus Nerve
CNXI - Accessory Nerve

265
Q

Cranial nerves which exit the skull via the hypoglossal canal

A

CNXII - Hypoglossal Nerve

266
Q

Function of nasal cavity

A

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

267
Q

Epithelium found in the nasal cavity

A 
Respiratory region (majority) - ciliated pseudostratified epithelium, interspersed with mucus secreting goblet cells.
Olfactory region (upper apex) - olfactory cells with olfactory receptors
268
Q

Function of nasal conchae

A

Increased surface area of nasal cavity, making airflow slow and turbulent.

Therefore, air remains in cavity longer for humidification

269
Q

Structures which open into nasal cavity

A

Sphenoid, ethmoidal, maxillary, frontal sinuses

Eustachian tube

Nasolacrimal duct

270
Q

Ethmoid Bulla

A

Opening of middle ethmoid sinus into nasal cavity

271
Q

Arterial supply to nasal cavity

A

Internal and external carotid arteries

272
Q

Venous drainage of nasal cavity

A

Pterygoid plexus
Facial vein
Cavernous sinus

273
Q

Kiesselbach Area

A

Anterior 1/3 of nasal cavity, common site of epistaxis (nosebleed) due to rich blood supply.

274
Q

Innervation of nose and nasal cavity

A

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.

275
Q

Significant risk associated with Cribriform plate fracture

A

CNS infection (meningitis, encephalitis, brain abscesses) since fractured cribriform plate can penetrate meningeal linings causing leakage of CSF.

276
Q

Anosmia

A

Loss of smell

Can occur due to damage of olfactory bulb in cribriform plate fracture.

277
Q

Vertebral level of larynx

A

C3-6

278
Q

Glottis of larynx contains

A

Vocal cords

279
Q

Interior surface of larynx is lined by…

A

Mucus membrane containing ciliated columnar epithelium

280
Q

Blood supply to larynx

A

Superior laryngeal artery (from superior thyroid)

Inferior laryngeal artery (from inferior thyroid)

281
Q

Function of true focal cords (Vocal laryngeal folds)

A

Control pitch of sound generated

282
Q

Reinke’s space

A

Found in vocal laryngeal folds. Contains fluid and GAGs which vibrate to create sound.

283
Q

Vestibular Laryngeal Folds

A

False vocal cords
Act to provide protection to larynx
Consist of vestibular ligament covered by a mucous membrane

284
Q

Action of suprahyoid muscles

A

Elevate larynx

285
Q

Action of infrahyoid muscles

A

Depress larynx

286
Q

Action of cricothyroid

A

Stretches and tenses vocal ligament - forceful speech

287
Q

Action of thyroarytenoid

A

Relaxes vocal ligaments - softer voice

288
Q

Muscles which alter size of rima glottidis

A

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

289
Q

Function of rima glottidis

A

Phonation - when air is forced through a closed RG, sound is generated.

290
Q

Tracheotomy

A

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.

291
Q

Indication for tracheotomy

A

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.

292
Q

Tracheostomy

A

An opening at the front of the neck so that a tube can be inserted into the windpipe - helping a person to breath.

293
Q

Origin of sternocleidomastoid

A

Sternum and clavicle

294
Q

Insertion of sternocleidomastoid

A

Mastoid process of temporal bone of the skull

295
Q

Function of sternocleidomastoid

A

Rotation of head and flexion of the neck

296
Q

Innervation of sternocleidomastoid

A

CNXI

297
Q

Complications of interscalene bloc

A

Temporary paresis of thoracic diaphragm (since phrenic nerve lies in this area)
Difficulty swallowing
Vocal cord paresis

298
Q

What is interscalene block?

A

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.

299
Q

Suboccipital muscles

A

Rectus capitis posterior minor and major

Obliquus capitis superior and inferior

300
Q

Actions of suboccipital muscles

A

Extension and rotation of head

301
Q

Structures found in the suboccipital triangle

A

Vertebral artery
Suboccipital venous plexus
Suboccipital nerve

302
Q

Action of stylohyoid muscle

A

Initiates swallowing by pulling hyoid postero-superiorly

303
Q

Innervation of stylohyoid

A

Stylohyoid branch of CNVII

304
Q

Action of digastric muscle

A

Depresses mandible and elevates hyoid bone

305
Q

Innervation of digastric muscle

A

Anterior belly - CNV

Posterior belly - CNVII

306
Q

Action of suprahyoid muscles

A

Elevate hyoid bone

307
Q

Scalene muscles:

Action:

Supplied by…

A

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)

308
Q

Jefferson Fracture

A

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)

309
Q

What type of cervical spine injury will result in spinal cord injury?

A

Dislocation or subluxation - 50% of cases occur at C6/7

310
Q

Hangman’s Fracture

A

Fracture of Pars articularis of axis (C2) due to rapid deceleration

311
Q

Significant risk of Dens Fracture

A

Unstable, at risk of avascular necrosis due to isolation of distal fragment from any blood supply.

312
Q

Bones which form the superficial border of the orbit

A

Frontal
Zygomatic
Maxillary

313
Q

Bones of the calvarium (vault of the skull)

A

Frontal
Parietal
Occipital

314
Q

Bones of the cranial base

A 
Frontal
Ethmoid 
Sphenoid 
Temporal
Parietal
Occipital
315
Q

Bregma

A

Anatomical point on the skull at which the coronal suture is intersected perpendicularly by the sagittal suture.
(Anteriosuperior)

316
Q

Lambda

A

Anatomical point on the skull at which the lumbdoid suture is intersected perpendicularly by the sagittal suture.
(Posterior)

317
Q

Arterial, Venous and nervous supply of dura mater

A

Middle meningeal artery and vein

CNV (trigeminal nerve)

318
Q

Arterial, Venous and nervous supply of arachnoid mater

A

Avascular

No innervation

319
Q

Arachnoid granulations

A

Projections of arachnoid mater into the dura which allow CSF to reenter circulation via dural venous sinuses

Year 2 (17 decks)

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