Neurosurgery Flashcards

Question

Abducens nerve palsy DDx

Answer 1

**1) Microvascular infarction** (DM, HTN) * *2) Raised ICP e.g. SOL, trauma** - false localising sign, thus ALWAYS check for papilloedema & raised ICP signs 3) Cavernous sinus syndrome, orbital apex syndrome

Answer 2

**Abducens nerve (CN VI)**, because: 1) Greatest intra-cranial length - thus prone to streching 2) The only nerve exiting from the dorsal brainstem 3) Compression against the petrous ligament or the ridge of the petrous temporal bone

Answer 3

Trigeminal nerve has 3 branches (OMM) -\> sensation and motor _1) Ophthalmic Branch (V1)_ * *Foramen**: superior orbital fissure * *Function:** - sensation to skin of forehead, scalp, eyelid, nose, cornea * *Branches:** - suprorbital, supratrochlear, lacrimal, infratrochlear, ethmoidal nerves _2) Maxillary Branch (V2)_ * *Foramen**: Foramen rotundum * *Function:** - sensation to skin of maxilla, upper lip, maxillary teeth and sinus _3) Mandibular Branch (V3)_ * *Foramen**: foramen ovale * *Function:** * sensation to skin over lower lip, mandible, anterior 2/3 of tongue * motor function of: - muscles of mastication - anterior belly of digastric, mylohyoid - tensor tympani - tensor veli palatini **Branches**: buccal, auriculotemporal, lingual, inferior alveolar nerves

Answer 4

CN VII _Function:_ * *1) Motor** - muscle of facial expression (see photo) - posterior belly of digastric, stylohyoid - stapedius * *2) Sensory** - Skin around external auditory meatus, tympanic membrane - sensation to soft palate - taste from anterior 2/3 of tongue * *3) Parasympathetic** - lacrimal glands, nasal glands - submandibular and sublingual glands _Course:_ - from pons at cerebellopointine angle - enters middle ear via internal auditory meatus; gives 3 branches: * Greater Petrosal Nerve (para to lacrimal -\> via pterygopalatine ganglion) * Chorda Tympani (taste to ant 2/3, para to saliva -\> via submandibular ganglion) * Nerve to Stapedius - travel along facial canel in petrous temporal bone - then exits via the stylomastoid foramen - enters parotid gland (most superficial) for terminal devisions: * Temporal * Zygomatic * Buccal * Marginal Mandibular * Cervical

Answer 5

UMN Lesion (supranuclear lesion or facial nucleus affected): 1) MCA cerebral infarction 2) AICA syndrome (lateral pontine syndrome) 3) Cerebral haemorrhage 4) Lacunar infarction, posterior limb internal capsule 5) Mass lesion

Answer 6

LMN lesion (i.e. facial nerve palsy): * *Common** 1) Bell's palsy (idiopathic) 2) Trauma * *Rare** 3) Tumour (e.g. acoustic schwannoma, cholesteatoma) 4) Diabetic mononeuropathy/ microvascular infarction 5) Ramsay Hunt syndrome (type II, caused by HZV in geniculate nucleus) 6) Lyme Disease 7) HIV 8) Sarcoidosis

Answer 7

CN VIII _Function: purely sensory_ * *1) Vestibular portion**: sensory for orientation and motion. * *2) Cochlear portion**: sensory for hearing _Course:_ - arises from the cerebellopontine angle - enters the ear via internal auditory meatus - then separates into vesticular and cochlear portions A fracture of the temporal bone may lead to injury of this nerve

Answer 8

_1) Physical Exam - Rinne and Weber tests_ - can be used as screening for unilateral deafness to distinguish between sensorineural and conduction hearing deficits. _2) Formal audiometry_ should subsequently be performed if there is clinical concern

Answer 9

CN IX _Function:_ * *1) Motor** - stylopharyngeus, lifting and opening pharynx * *2) Sensory** - Taste and sensation to posterior 1/3 of tongue - Sensation to palate, pharynx (afferent of gag reflex) * *3) Parasympathetic** - Parotid gland (via the otic ganglion) _Course:_ - exits via the jugular foramen

Answer 10

_Function_ * *1) Motor** - pallatoglossis of tongue - pharynx, larynx, upper esophagus, palate * *2) Sensation** - skin behind auricle - pharynx, larynx - trachea, bronchi - heart - esophagus, stomach, intestines * *3) Parasympathetic** - smooth muscles of thoracic and abdominal organs _Course:_ - arises from medulla - exits via jugular foramen - joined by cranial accessory nerve - pass down within carotid sheath, behind and between IJV and common carotid - at the neck, give rise to right RLN that hooks around right subclavian artery - at the thorax, give rise to left RLN that hooks around the aortic arch, also cardiac branches - then travel at left and right of esophagus, enters abdomen via esophageal hiatis (T10) - left vagus nerve becomes anterior vagal trunk, right becomes posterior

Answer 11

CN XI * *1) Spinal root** - function: purely motor, SCM and trapezius - course: originate from cervical plexus, enter cranium via foramen magnum, leave through jugular foramen * *2) Cranial root** - function: joins the vagus nerve - course: originate from medulla, exits cranium via jugular foramen

Answer 12

_CN XII_ * *Function: pure motor** - supplies all intrinsic and extrinsic muscles of the tongue, except palatoglossus (PG) * *Course:** - originate from medulla - exits through hypoglossal canal

Answer 13

**1) Brainstem lesions** * *2) Orbital Apex Syndrome** - CN II, III, IV, V1, VI * *3) Cavernous sinus syndrome** - CN III, IV, V1, V2, VI * *4) Cerebellopontine angle tumour** - CN V, VII, VIII (+ jugular foramen IX, X, XI)

Answer 14

The right is a branch of the brachiocephalic trunk The left comes directly off of the aortic arch

Answer 15

_A. Course in Neck:_ - starts at the bifurcation of common carotid artery (level C4) - origin is dilated, forming the carotid sinus - initially lateral to ECA, then becomes medial and posterior to it - continue travel up with IJV in the carotid sheath - passes under posterior belly of digastric muscle and parotid gland to enter base of skull - no branches in neck _B. Course in Skull_ - enters cranium via carotid canal (in petrous temporal bone) - tortuous course with six bends (to relieve pressure effect on the delicate cerebral tissue) - enters cavernous sinus (lies in the medial wall), after which it turns back on itself to pass medial to the anterior clinoid process (of the sphenoid bone). - give rise to branches: * Opthalmic artery (forst branch after ICA emerge from cavernous sinus, exits via optic canal) -\> supratrochlear and supraorbital branches, central retinal artery * Anterior cerebral artery * Middle cerebral artery * Posterior communicating artery

Answer 16

Carotid sinus is the dilated origin of the internal carotid artery at the bifurcation (C4 level). It is richly innervated by the glossopharyngeal nerve (CN IX). Carotid body is the chemoreceptor at the carotid sinus. _Acts as a baroreceptor and chemoreceptor:_ - if high BP, then vagal mediate to decrease HR, peripheral vasodilation - if high CO2 or low O2, then vagal mediate to increase respiratory rate

Answer 17

_Vertebral artery:_ - originates from the subclavian artery - crosses the apex of the lung - enters the transverse foramina of vertebrae C1-6 - enters the cranium via foramen magnum, piercing the dura mater - runs on anterolateral surface of medulla to join with the contralateral vertebral artery - form basilar artery into the circle of Willis _Important branches (actually Basilar artery branches):_ 1) Anterior spinal artery 2) Posterior spinal artery 3) Anterior and posterior inferior cerebellar artery 4) Superior cerebellar artery 5) Pontine branches 6) Posterior cerebral artery 7) Basilar artery -\> inferior cerebellar arteries also gives off the labyrinthine arteries that supply the inner ear via the internal acoustic meatus

Answer 18

Formed from the union of the two vertebral arteries. It lies on the clivus (part of the cranium at the base of the skull).

Answer 19

Circle of Willis = anastomosis between the internal carotid arteries anteriorly and the vertebral arteries posteriorly, located within the cranium and forming the major blood supply to the brain. It is found at the base of the brain in the region of the optic chiasma and the pituitary stalk

Answer 20

The pituitary stalk gives rise to the pituitary gland which sits in the sella turcica in the middle cranial fossa. Note that this is surgically accessible through a transphenoidal approach via the sphenoid sinus

Answer 21

At the point at which a cerebral artery branches off the circle of Willis. They can rupture and bleed. They are associated with polycystic kidney disease.

Answer 22

2 drainage systems: * *1) Dural sinuses** - drains superficial structures (e.g. cerebral or cerebellar cortex) * *2) Internal cerebral vein** - choroid vein (drains choroid plexus) and thalamostriate vein joins to form internal cerebral vein at the interventricular foramen

Answer 23

These are areas where the outer periosteal layer of the dura mater becomes separated from the inner meningeal layers. These contain venous blood and are lined with endothelium. Examples: * *1) Superior sagittal sinus** - begins anteriorly at the crista galli, then along superior part of falx cerebri - ends in the right transverse sinus - connects many venous lakes with the archnoid granulation (thus filter CSF back to blood) * *2) Inferior saggital sinus** - lies in free margin of falx cerebri - ends into straight sinus to left transverse sinus * *3) Straight sinus** - runs in the junction of the falx cerebri and the tentorium cerebelli - formed by junction of great cerebral vein and inferior saggital sinus - continues into left transverse sinus * *4) Transverse sinus** - in lateral part of tentorium cerebelli, start at internal occipital protuberance - on reaching mastoid temporal bone, it forms the sigmoid sinus * *5) Sigmoid sinus** - emerge through the jugular foramen as IJV **6) Petrosal sinus** **7) Cavernous sinus**

Answer 24

- The superior sagittal sinus drains into the right transverse sinus. - The inferior sagittal sinus drains into the straight sinus to continue as the left transverse sinus. - The superior petrosal sinus drains into the transverse sinuses, connecting the cavernous sinus

Answer 25

Sagittal sinus thrombosis may arise from: - Skull, nose, face, scalp infections, via diploic or emissary vein connections

Answer 26

There are no valves in the sinuses or in the veins which connect to them. This makes them vulnerable to infection, as bidirectional blood flow is possible.

Answer 27

There is a superior petrosal sinus and an inferior petrosal sinus. The superior sinus runs in the edge of the tentorium cerebelli and connects the cavernous sinus with the transverse sinus. The inferior petrosal sinus runs between the occipital bone and the temporal bone, connecting the cavernous sinus and the internal jugular vein.

Answer 28

Cavernous sinus is a paired structure found lateral to the body of the sphenoid bone (at the sella turcica) It has a cavern-like appearance filled with blood. It drains from the superficial middle cerebral, superior and inferior ophthalmic veins and the sphenoparietal sinuses. _Borders:_ 1) Medial: Sphenoid bone / sphenoid sinus 2) Superior (Roof) and Lateral: Meningeal layer of Dura 3) Inferior (Floor): Endo-osteal layer of Dura 4) Anterior: Superior orbital fissure 5) Posterior: Petrous temporal bone

Answer 29

_Running through it:_ 1) ICA and CN 6 traverse the sinus 2) CN 3, 4, V1, V2 runs in the lateral wall * *aka "OTOM CAT"** - Lateral (sup to inf): Occulomotor, Trochlear, Opthalmic, Maxillary - Superior (med to lat): Internal Carotid, Abducens _Receives:_ * *1) Opthalmic veins** (which links **pterygoid venous plexus** and **anterior facial vein**) * *2) Superficial Middle Cerebral Vein** (Brain venous drainage) * *3) Sphenoparietal sinus** (dura drainage) _Connection:_ * *1) Superior petrosal sinus** to Right transverse sinus * *2) Inferior petrosal sinus** to Internal jugular vein

Answer 30

The occulomotor nerve (CN III), trochlear nerve (CN IV), the ophthalmic and maxillary branches of the trigeminal nerve (CN V1 and CN V2) "OTOM CAT"

Answer 31

* *1) Facial infections** - infection may spread through the facial vein - a triangle formed by the upper lip, nose, medial cheek and medial eye that is drained via the inferior ophthalmic vein to the cavernous sinus **2) Deep infection** via pterygoid venous plexus around the pterygoid muscles

Answer 32

Skin Connective tissue (dense) Aponeurotic layer Loose areolar connective tissue Periosteum

Answer 33

From the **inferior petrosal sinus** and the **sigmoid sinus** forming the internal jugular vein, this exits the skull through the jugular foramen. The transverse sinuses drain into the sigmoid sinus which forms an S-shape to pass to the jugular foramen. The inferior petrosal sinus connects and drains the cavernous sinus into the internal jugular vein.

Answer 34

Cerebral cortex is divided into four lobes by 2 major sulci and 2 imaginary lines: - Central sulcus (Rolandic fissure): frontal from parietal - Lateral sulcus (Sylvian fissure): frontal from temporal - Line from parieto-occipital sulcus to pre-occipital notch: parietal from occipital - Line horizontally from posterior end of sylvian fissure: parietal from posterior temporal Lobes being: 1) Frontal 2) Parietal 3) Temporal 4) Occipital

Answer 35

_Frontal Lobe_ - intellectual activity - emotion - voluntary movements (Primary motor cortex at pre-central gyrus) - speech (Broca's area at inferior frontal gyrus of dominant hemisphere) _Parietal lobe_ - somatic sensation (primary sensory cortex at post-central gyrus) - integration of sensory stimuli with other information (parietal association cortex) _Temporal Lobe_ - Hearing (primary auditory cortex at superior temporal gyrus) - Integration of auditory stimuli with other sensory information (temporal association region) _Occipital Lobe_ - Vision (visual cortex)

Answer 36

It is a massive band of white matter that connects the left and right cerebral hemispheres, spanning the length of the longitudinal fissure of the brain

Answer 37

1) Ataxia 2) Nystagmus 3) Dysdiadochokinesia 4) Intention tremor

Answer 38

Cerebellum connected to brainstem via 3 pairs of cerebellar peduncles: * *1) Superior cerebellar peduncles** - to midbrain - transmits efferent fibres to midbrain and thalamus * *2) Middle cerebellar peduncles** - to pons - relays input from higher centres via pontine nucleus * *3) Inferior cerebellar peduncles** - to medulla - relays input from vesticular nucleus, spinal cord, and inferior olivary nuclei

Answer 39

Basal Ganglion: 1) Putamen, globus pallidus (lentiform nucleus) 2) Caudate nucleus 3) Claustrum _Function:_ - caudate nucleus and putamen receive afferent from cerebral cortex and thalamus - send efferent to globus pallidus - globus pallidus send efferent to thalmus, red nuclei, substantia nigra, reticular formation - for planning and regulation of complex voluntary movements, and learning of motor skills

Answer 40

* *1) Midbrain** - formed by two parts: tectum and the paired cerebral peduncles - Internally they are separated by the substantia nigra into the crus cerebri and tegmentum - CN III (from interpeduncular fossa), CN IV - Pineal gland located at dorsal surface, secretes melantonin * *2) Pons** - CN V, CN VI (arises from ventral surface), CN VII, CN VIII * *3) Medulla oblongata** - CN IX, CN X, CN XI, CN XII

Answer 41

The midbrain is associated with the accommodation and pupillary light reflexes: _1) Light reflexes_ - Retina sends signal to optic nerve. Fibres from **optic tract** enters superior colliculus and syncapse on the pretectal nucleus (no need go through occipital visual cortex) - Fibres pass bilaterally towards the Edinger–Westphal nuclei - parasympathetic fibres (via CN3) then head to the ciliary ganglion and, subsequently, the constrictor pupillae. _2) Accommodation reflex_ - light on each retina is taken to the occipital lobe via the optic nerve -\> optic tract -\> optic radiation - **Cortico-tectal fibres** travel through the superior colliculus and synapse on the pretectal nucleus - Fibres pass bilaterally towards the Edinger–Westphal nuclei - parasympathetic fibres (via CN3) then head to the ciliary ganglion and, subsequently, the ciliary muscles, constrictor pupillae

Answer 42

This contains the descending motor fibres i.e. corticospinal and corticobulbar fibres which control movement through the cranial nerves and in the peripheral nervous system

Answer 43

4th ventricle

Answer 44

Corneal reflex = involuntary blinking of the eyelids elicited by stimulation of the cornea: 1) Sensory afferents: from the **ophthalmic division of the trigeminal nerve** (CN V1) 2) It synapse in the trigeminal sensory nucleus in the pons 3) Fibres then travel to the ipsilateral facial motor nucleus in the pons 4) Motor efferents: sent via facial nerve to orbicularis oculi (zygomatic branches)

Answer 45

* *Descending motor**: The lateral corticospinal (pyramidal) tract decussates at the medullary pyramids. - \> controls peripheral muscles (limbs) * *Ascending sensory**: The dorsal column–medial lemniscus pathway - \> fine touch, vibration, two-point discrimination, and proprioception

Answer 46

**The area postrema.** - \> the permeability allows it to act as the chemoreceptor trigger zone (CTZ) for vomiting - \> contact time for blood-borne hormones to interact with neuronal receptors involved in regulation of blood pressure, body fluids

Answer 47

Gag reflex: 1) Sensory Afferents: from the pharynx travel in the **glossopharyngeal nerve** (CN IX) 2) Travels to the **nucleus solitarius** of the medulla 3) Connections to the **nucleus ambiguus** of the vagus nerve at medulla 4) Motor efferents: sent via the vagus nerve to the **pharyngeal muscles and soft palate**.

Answer 48

Reticular formation

Answer 49

There are four interconnected ventricles. There is a left and right lateral ventricle (one for each hemisphere), the third ventricle and the fourth ventricle. Interventricular foramina (of Monro) connects the lateral ventricles to the third ventricle. Cerebral aqueduct (of Sylvius) connects the third ventricle to the fourth ventricle

Answer 50

_1) Lateral Ventricles_ - largest ventricles, lie deep in cerebral hemispheres - Consists of frontal horn, body, occipital horn, temporal horn - Foramen of Monro is inferior to the frontal horns _2) 3rd Ventricle_ - thin, slit like ventricle - bound laterally by thalamus, inferiorly by hypothalamus _3) 4th Ventricle_ - diamond shaped ventricle - Anterior wall = pons and medulla - Superior roof = cerebellar hemispheres, superior and inferior medullary vela

Answer 51

The foramen of Luschka

Answer 52

**1) Mechanical shock absorption as cushion** * *2) Suspension of brain in fluid** - to reduce effective weight of the brain - prevent curshing of lower portion of brain under its own weight - protection from sudden pressure change * *3) Nutrition & elimination of waste** - delivers glucose to brain * *4) Biochemical homeostasis** - regular ion composition and pH * *5) Immunological** - circulating immunological factors

Answer 53

_Composition:_ Normally crystal clear, containing: * *1) Water 2) Protein, glucose** (less than plasma) * *3) Small amount of white cells 4) Electrolytes** - More Na, Cl and H+ ions than plasma - Less Ca, K than plasma _Volume_: around 150ml

Answer 54

* *Production:** - Around 500ml per day - 70% from Choroid plexuses of the lateral, 3rd & 4th ventricles - 30% from directly from vessels lining the ventricular wall * *Circulation:** - lateral to 3rd ventricle via foramina of Monro (interventricular foramina) - 3rd to 4th ventricle via aqueduct of Sylvius - 4th to subarachnoid space of spinal cord via foramen of Magendie (medial) & 2 foramina of Luschka (lateral) - After going around the spinal cord, it enters the cranial cavity through the foramen magnum, and flows around the brain within the sub-arachnoid space. * *Re-Absorption:** - 80% re-absorbed by arachnoid granulations at dural venous sinuses, passively under CSF pressure - 20% is absorbed at the spinal nerve roots

Answer 55

Blood -brain barrier controls the entry of substances into the extra-cellular fluids of the CNS and the rate of entry. It is formed by: **1) Tight junctions** (zona occludens) between the endothelial cells of the cerebral capillaries. **2) Astrocytic foot processes** applied to the basal membranes of the cerebral capillaries - Fat crosses easily, with fat soluble drugs (opiate, anaesthetics) - Glucose can also cross - Hydrogen ion do not usually cross

Answer 56

It is absent in a few areas: * *1) Median eminence of hypothalamus** - where hypothalamic neurons release hormones into the portal system, in order to act on the anterior pituitary * *2) Posterior pituitary (Neurohypophysis**) - ADH and oxytocin are released by neurons directly into the blood * *3) Circumventricular organs** adjacent to 3rd and 4th ventricles - the area is adjacent to the chemotrigger zone - such as the supraoptic crest, the area postrema and tuber cinerium

Answer 57

BBB integrity is affected by: infection, tumours, trauma, and ischaemia.

Answer 58

Classified based on communicating or not, and aetiology _COMMUNICATING:_ * *1) Congenital** - arnold chiari malformation - encephalocele * *2) Acquired** - normal pressure hydrocephalus (60% no known aetiology) - Infective (e.g. meningitis or post-meningitis) - SAH or IVH - Cenous hypertension, sinus thrombosis - Hydrocephalus ex vacuo (due to post stroke volume loss) - over-production e.g. choroid plexus papilloma _NON-COMMUNICATING:_ * *1) Congenital** - Aqueduct stenosis - Dandy Walker malformation (atresia of foramen of Magendi and Luschka) - Vascular malformation * *2) Acquired** - tumours (e.g. at 3rd ventricle, posterior fossa, pineal region) - aqueductal haematoma - abscess - ventricular scarring

Answer 59

Depends on neonate vs adults _Neonates:_ - Bulging fontanelles - Prominent scalp veins - Sunset eyes (due to CSF pressure over midbrain tectum) - Papilloedema - Disproportionate head growth - Irritability, developmental delay _Adults:_ - Raised ICP symptoms: headache, nausea, vomiting, drowsiness, papilloedema - Loss of upward gaze - Cognitive impairment, poor concentration

Answer 60

_Classical triad symptoms of:_ 1) Dementia 2) Gait ataxia 3) Urinary incontinence _Causes:_ 1) Mostly idiopathic (60%) 2) Arise insidiously after SAH 3) Arise insidiously after meningitis

Answer 61

* *1) CT, MRI** to look for: - periventricular oedema - enlargement of temporal horns (\>2mm), lateral ventricles, and 3rd ventricles - obliteration of basal cistern and cortical sulci * *2) Cranial USG** in infant - if fontanelles are open

Answer 62

Definitive management is by: _A. External Drainage of CSF_ * *1) Lumbar puncture and lumbar drain** - as temporary CSF drainage until normal circularion/resorption - only be considered in communicating hydrocephalus - avoid over-drainage -\> may lead to SDH or cerebellar tonsillar herniation * *2) External Ventricular Drainage (EVD)** - used in acute setting (e.g. SAH) when hydrocephalus is trasient, in order to avoid permanent shunt - used as temporaizing measure if high particulate content of CSF increase risk of early shunt blockage (e.g. protein in post-meningitis, or blood in IVH) - can use to administer intrathecal medication for treatment of ventriculitis _B. Permanent Shunting_ * *1) VP Shunt (ventriculo peritoneal)** - commonest shunt, from proximal catheter at lateral ventricle, to distal catheter tunneled to the abdomen which is inserted to peritoneal cavity * *2) VA Shunt (ventriculo atrial)** - if VP shunt not preferred (e.g. extensive abd surgery, peritonitis, morbid obesity) - distal catheter inserted via jugular vein to SVC * *3) LP Shunt (lumbo peritoneal)** - only for communicating hydrocephalus _C. Ventriculostomy_ **1) Endoscopic third ventriculostomy** _D. Medical Treatment (only in selected circumstances for temporalizing)_ * *1) Osmotic diuretics (e.g. mannitol)** - as temporizing measure in acute setting e.g. blocked shunt * *2) Acetazolamide (carbonic anhydrase inhibitor)** - inhibits CSF production - often used in benign intracranial hypertension in neonates, as temporizing measure while the child gains weight prior to shunt procedure

Answer 63

1) Obstruction / Blockage 2) Dislodgement / Breakage / Erosion 3) Infection 4) Seizure 5) Overshunting, may cause subdural haematoma _Ventriculo-peritoneal shunt (for hydrocephalus):_ 6) Abdominal complications e.g. pseudo-cyst _Ventriculo-atrial shunt:_ 6) Shunt embolism 7) Short catheter length (requires repeated lengthening in growing child) 8) Perforation 9) Pulmonary HTN

Answer 64

**Adult**: normally 10 -15 mmHg **Raised ICP**: Elevation of mean CSF pressure above 15mmHg when measured in lateral decubitus position

Answer 65

Intracranial content = blood + CSF + Brain In case of increasing ICP, compensated in this order: i) venous blood ii) CSF iii) brain

Answer 66

**1) Reduced venous blood** volume in brain **2) Decreased CSF volume** **+) Infant**: separation of sutures, bulging fontanelles **3) Long term**: skull bone erosion, brain atrophy

Answer 67

This shows the changing nature of the compliance of the intracranial contents with increases in the ICP. Initially, due to a higher intracranial compliance, a small rise in the volume leads to little rise in the ICP. At a higher volume, there is an exponential rise in the ICP owing to the contents becoming ‘stiffer’ due to volume overload. The volume at which this ICP decompensation occurs differs among individuals.

Answer 68

Cerebral Perfusion Pressure = Mean arterial pressure - intracranial pressure = MAP - ICP

Answer 69

CBF = CPP/CVR where CPP = cerebral perfusion pressure CVR = cerebrovascular resistance (Radius⁴; Length; Viscosity)

Answer 70

Between systolic pressures of 50–150mmHg, the cerebral blood flow remains constant owing to local autoregulation of flow. Auto-regulation achieved by: * *􏲹1) Myogenic response** of the arteriolar smooth muscle cells: - MAP increases -\> increase wall tension - \> stimulate reactive contraction of the cells - \> thus increase cerebral vascular resistance * *2) Vasodilator "Washout"** - if blood flow is increased due to increased MAP - \> locally produced vasodilators are washed out - \> thus decreased vasodilation - \> thus increased cerebral vascular resistance _Factors affecting cerebral blood flow:_ * *1) Systemic arterial pressure 2) CO2:** - hypercarbia increases CBF due to increase H+ - hypocarbia leads to cerebral vasoconstriction * *3) Hypoxia**: causes vasodilation * *4) 􏲹Sympathetic innervation of cerebral vessels**: this has a minor effect on the cerebral flow

Answer 71

This is mixed vagal and sympathetic stimulation that occurs in response to an elevated ICP. It leads to the Cushing's triad: * *1) Hypertension** -\> to ensure an adequate cerebral perfusion pressure * *2) Reflex bradycardia 3) Irregular respiration**

Answer 72

_Initial symptoms:_ * *1) Headache** worse in morning (meningeal stretching) * *2) Nausea, Vomiting** (brainstem distortion) * *3) Confusion, impaired consciousness** - as ICP increases, there is decreased cerebral blood flow _Signs:_ * *4) Decrease GCS 5) Cushing's Reflex at a later stage** - Hypertension - Bradycardia - Irregular respiration * *6) Papilloedema 7) Cranial nerve palsy:** - Unilateral mydriasis (dilated pupils from CN III lesion) - Diplopia (CN VI lesion) ----------------------------------- if untreated - Cerebral ischemia - Coma - Brain herniation - Brainstem compression - Respiratory arrest - Certain Death

Answer 73

This occurs in raised ICP because the occulomotor nerve is pushed against the free edge of the tentorium and is a sign of impending tentorial herniation (coning). The fibres that are damaged are the parasympathetics that travel with the third nerve from the Edinger–Westphal nucleus in the midbrain to supply sphincter pupillae, leading to unopposed sympathetic dilatation of the pupil. Without a CT, in a suspected extradural haematoma, a burr hole would be drilled on the same side as the pupil. However, in some cases the opposite side can be dilated (false localizing sign).

Answer 74

Practically, consider the reversible causes first: - Fever - Seizure - Infection - Inadequate sedation - Electrolyte disturbances - Hypercapnia Based on Monro-Kellie Doctrine: _A. Increased CSF_ * *1) Hydrocephalus** (obstructive vs communicating, congenital vs acquired) - see hydrocephalus DDx _B. Increased Blood_ * *2) Intra-cranial bleeding** - Extra-dural, subdural, subarachnoid, intracerebral, intraventricular **3) Hyperaemia** * *4) Venous sinus obstruction** - cerebral venous thrombosis - Trauma with fractures overlying sinus _C. Increased Brain_ * *5) Mass lesions** - Tumour - Infection (cerebral abscess, empyema, tuberculoma, hydatid cyst) * *6) Brain Swelling (Cerebral oedema)** - Cerebral Contusion, Diffuse Axonal Injury - Vasogenic (e.g, SAH, cerebral inschemia) - Metabolic i.e. hyponatremia - Cytotoxic (e.g. encephalitis, meningitis) - Hydrocephalic

Answer 75

**1) Obliteration of the cortical sulci / basal cistern** **2) Midline shift / cerebral herniation** from pressure effect * *3) Features of hydrocephalus** - enlargement of the temporal horn \>2mm - enlargement of the 3rd ventricle - periventricular oedema

Answer 76

1) BP/P, Saturation, respiratory rate, ABG, urine output 2) GCS monitoring if conscious 3) ICP monitoring if unconscious 4) Transcranial Doppler 5) Study of metabolism

Answer 77

* *_Indicated in head trauma patient if:_** - No reliable clinical monitoring (e.g. sedation & coma) - GCS less than 8 - Abnormal CT - Normal CT, but presence of \>2 risk factors * Age \>40 * SBP \<90 * Focal neurological deficit (unilateral or bilateral motor posturing) * *_Contraindication_** - Conscious patient - Coagulopathy

Answer 78

_A. Invasive methods_ * *1) Ventricular monitoring (Gold Standard)** - External ventricular drain (EVD) or ventriculostomy - passed into the anterior horn of the lateral ventricle via usually a frontal burr hole * *2) Brain parenchymal ICP transducer ("microsensor")** - through a cranial access device (usually referred to as ‘a bolt’) - Use when ventricle is too difficult to puncture e.g. too small or having bleeding tendency **3) Subdural catheter**: little used now and has been shown to correlate poorly with ‘actual’ ICP **4) Palpation of a craniotomy flap** when the bone is left out (obviously not very accurate but can be a useful sign if there is no ICP monitor in situ). _Non-invasive methods_ 5) Not well validated but **transcranial Doppler** (TCD) can be used to measure velocities in the middle cerebral artery and derive a ‘pulsatility index’ that may correlate with ICP. 6) Jugular venous O2

Answer 79

Two main reasons: 1) A high ICP can lead to **cerebral herniation** - may lead to rapid onset of coma, respiratory failure, and death. 􏲹2) A high ICP causes a **reduction of the cerebral perfusion pressure** (CCP = MAP - ICP)

Answer 80

_Initial management (to buy time)_ * *1) Resuscitation (ABC)** - intubation if airway not protected - consider inotropes to maintain MAP to increase CPP (if not traumatic) * *2) Look for reversible causes**, i.e. - fever - seizure (if sedated may need EEG) - infection - hypercapnia - inadequate sedation * *3) Enhanced venous drainage** - avoid neck rotation, remove neck collar (if not indicated) - Head elevation (~30-40º) * *4) Diuretics** - IV 20% mannitol (200ml) - can also consider frusemide * *5) Controlled hyperventilation** - decreases PaCO₂ to ~4.5 kPa, thus causing certain vasoconstriction of cerebral arteries * *6) Controlled hypothermia** - reduce basal metabolic rate * *7) Sedation (Barbiturate coma)** - with phenobarbitol, thiopentone - Decreases Neuronal activities & cerebral metabolism, thus lowering cerebral blood flow and ICP - Monitor EEG * *±8) Dexamethasone** - Reduce cerebral edema for tumour and infection only _Emergency Surgical Managment:_ * *1) CSF drainage** if hydrocephalus - EVD **2) Decompressive craniectomy +/-􏰇 evacuation of mass lesions, evacuation of clot** **±3) Lobectomy for intractably raised ICP**

Answer 81

PaCO₂ should be kept around 4.5 kPa - if too low, vasoconstriction will be too pronounced, causing an increase in Cerebrovascular Resistance (CVR), which then greatly decreases the Cerebral Blood Flow, causing greater neurological deficits

Answer 82

Note that traumatic brain injury might destroy vasoreactivity: While normally increasing MAP will reduces ICP while keeping CBF relatively constant; With vasoreactivity gone, raised MAP will increase CBF and increases the ICP -\> therefore don't raise the MAP!

Answer 83

2 classes: _A. Supratentorial Herniation_ * *1) Transtenorial**: - usually uncal herniation: the uncus of the temporal lobe passes through the tentorial hiatus - but can also be central herniation * *2) Subfalcine / Cingulate** - where the cingulate gyrus herniates beneath the falx cerebri * *3) Transcalvarial** (Fungus) * *4) Tectal** _B. Infra-tentorial Herniation_ * *5) Reverse transtentorial 6) Tonsillar herniation** (i.e. Coning) - leading to displacement of the medulla and the cerebellar tonsils through foramen magnum. Compression of the respiratory centre leads to respiratory depression 1) Subfalcine/ supra-callosal / Cingulate 4) cerebellar tonsil herniation (coning) 5) transcalvarial/ fungus 6) Central

Answer 84

i.e. Transtentorial herniation of uncus of temporal lobe, which will compress the following: * *1) Ipsilateral CN III** - _ipsilateral mydriasis_ - _downward outward eye_ * *2) CN I and retinal vein** - _papilloedema_ * *3) Posterior cerebral artery** - \> ipsilateral occipital cortex infarction -\> _cortical blindness_ **4) Aqueduct of sylvius** -\> hydrocephalus **5) Midbrain and pontine** infarction and haemorrhage (loss of consciousness, bradycardia, respiration changes, hypertension, may even cause decorticate & decerebrate postures) **6) Contralateral hemiplegia** * *7) Kernohan's notch** - contralateral cerebral peduncle pushed against tentorium -\> _ipsilateral hemiplegia_ (*false localising sign*)

Answer 85

i.e. Downward displacement of diencephalon trans-tentorially, causing: ## Footnote **1) Bilateral miosis** **2) Cheyne-Stokes respiration** **3) Loss of consciousness**

Answer 86

Displacement of cerebellar tonsils through foramen magnum (aka coneing), causing: **1) Cardiorespiratory arrest** (from medulla distortion) **2) Impaired consciousness** **3) Decorticate posture** (flexed; above red nucleus) --\> **decerebrate posture** (extended, below red nucleus)

Answer 87

* *1) CN VI Palsy** - long intra-cranial route - may be compressed against the petrous ligament on the ridge of the petrous temporal bone * *2) CN III Palsy** - transtentorial uncal herniation may compress CN III against free edge of tentorium * *3) Kernohan's notch** - transtentorial uncal herniation may compress contralateral cerebral peduncle pushed against tentorium - thus ipsilateral hemiparersis

Answer 88

_Motor, Verbal, Eye_ ``` M6 = obey command M5 = localise pain M4 = withdraw to pain M3 = abnormal flexion to pain M2 = extend to pain M1 = no movement ``` ``` V5 = Oriented to TPP V4 = Confused speech V3 = Inappropriate words V2 = Incomprehensible sounds V1 = no speech ``` ``` E4 = spontaneous eye movement E3 = open to command E2 = open to pain E1 = not open ```

Answer 89

_Based on GCS ("3, 4, 5")_ Mild head injury (GCS 13-15) Moderate head injury (GCS 9-12) Severe head injury (GCS 3-8)

Answer 90

Depends on sensorium: If orientated = 1 in 6000 If disorientated = 1 in 120

Answer 91

* *1) Mechanism and timing of trauma** - any safety equipments (e.g. seatbelt, helmet) * *2) Consciousness** - any LOC, any confusion **3) Any Seizure** **4) Symptoms of elevated ICP** (headache, N, V) **5) Neurological deficits**

Answer 92

Low threshold in head trauma: 1) Any drop in GCS 2) Seizure, focal neurological deficits 3) Penetrating skull injury, skull fracture 4) Known coagulopathy

Answer 93

_A. ATLS, stablisation of patient_ * *1) ABC, primary survey** - may require intubation and ventilation * *2) Secondary survey** _B. Evaluation and investigations_ * *3) Bloods tests and CT Brain** for severity of primary brain injury - low threshold for repeated imaging _C. Temporary management of any high ICP_ * *4) Mechanical method**, look for reversible causes * *5) Hyperventilation 6) Hypothermia 7) Diuretics, barbituate coma** _D. Other managment_ * *8) Seizure prophylaxis 9) Stress ulcer prophylaxis 10) Optimise nutrition 11) Manage hyperthermia** - due to hypothalamic dysfunction or infection * *12) Manage hyponatremia** with careful fluid and electrolyte balance - HypoNa is common due to SIADH, stress response to trauma with Na & water retention, and overhydration _D. Early liasion with neurosurgical unit and ICU_ _E. Definitive surgical management if needed_

Answer 94

_A. Acute / Short term_ * *1) Scalp laceration 2) Skull fracture, base of skull fracture 3) Brain contusion, diffuse axonal injury 4) ICH** (EDH, SDH, SAH) * *5)􏲸 Meningitis and brain abscess**: if there is an open communication _􏲹B. Chronic / Longer term_ **1) Epilepsy**: especially common in the situation of a depressed fracture, intracranial haematoma or prolonged amnesia **2) Hydrocephalus**: caused by obstruction from an intraventricular haemorrhage **3) Chronic subdural haematoma**: may cause symptoms from a chronic elevation of the ICP, and managed by surgical evacuation * *􏲸4) Cognitive symptoms**: - post traumatic amnesia - post concussion syndrome e.g. persisting headaches, dizziness and poor concentration

Answer 95

* *Presentation:** - Usually post head injury - Classical lucid interval - Symptoms of raised ICP * *Anatomy:** - break of the temporal bone -\> bleeding from the middle meningeal artery - not necessarily associated with cortical damage if evacuated in a timely manner * *CT findings:** - Convex, len-shaped haematoma - Does not cross sutures (because EDH strip pericranial dura away from skull), can cross tentorium - Often associated skull fracture - Coup lesion, may have countrecoup subdural - Midline shift if large

Answer 96

* *0) Management of traumatic head injury** first - ATLS, resuscitation - management of raised ICP _Definitive treatment:_ * *1) Acute craniotomy + Clot evacuation** - not necessarily associated with cortical damage if evacuated in a timely manner

Answer 97

SDH: * *Presentation:** - usually post traumatic injury * *Anatomy:** - due to tearing of dural bridging veins; thus especially in elderly with brain atrophy - indicates underlying cortical damage (mass effect increases ICP) **CT findings:** - crescentic haematoma - can cross suture lines, does not cross tentorium - flattens the sulci - mass effect, midline shift, significant oedema - Density depends on timing: \> swirling lucency if active bleeding \> hyperdense if acute (\<1 week) \> isodense if sub-acute (1-3 week) \> hypodense if chronic (\>3 weeks)

Answer 98

* *0) Management of traumatic head injury first** - ATLS, resuscitation - management of raised ICP _Definitive treatment:_ * *1) Acute craniotomy + Clot evacuation** - if acute SDH and midline shift \>1cm **2) Burrhole** if chronic SDH

Answer 99

_Brain Contusion_ * *1) Presentation** - from traumatic head injury - delayed drop in GCS due to evolution of haematoma - raised ICP Sx * *2) Mechanism**: - mechanism often from rapid deceleration of the brain against the inside of the cranium * *3) CT findings**: - coup countre-coup is common - Bifrontal contusions is common - Initial CT: maybe normal, under-estimate the eventual size of contusion - 24-48 hour CT: new and larging lesion, "salt and pepper" appearance ==\> therefore repeat CT is low threshold

Answer 100

Diffuse axonal injury * *Mechanism:** - high energy impact/deceleration - \> causing shearing of the white matter against the grey matter, thus significant fibre disruption - \> parenchymal disruption, thus generalised cerebral oedema, increased ICP * *Presentation** - after traumatic head injury (usually high energy) - may have prolonged coma - poor prognosis * *Radiological Findings:** - CT often initially normal - Need MRI to note petechial haemorrhage

Answer 101

**1) Battle's sign, haemotympanum** **2) CSF otorrhoea** * *3) CSF rhinorrhoea** - due to mastoid fracture, but intact eardrum therefore CSF flow to nose through Eustachian tube * *4) Racoon eyes** - indicates skull fracture over anterior cranial fossa - NEVER put in a Ryle’s tube through nose, or else go to brainstem

Answer 102

**1) CN palsy**: 1, 2, 6, 7, 8 **2) CSF leakage, meningitis** **3) Traumatic aneurysm** **4) Carotid-cavernous fistula** (delayed presentation, swollen red eye)

Answer 103

* *1) Conservative management** - Bedrest for 5-7 days - CSF leak usually spontaneously resolve within 2 weeks **2) Consider prophylactic antibiotics** in some units **3) Operative repair** in some cases

Answer 104

Burr holes are used for procedures that require _limited intracranial access_: * *1) Immediate Relief of acute EDH or SDH** - before performing a formal craniotomt + clot evacuation **2) Treatment of chronic SDH** * *3) Placement of ventriculostomy catheter** - e.g. external ventricular drain **4) Placement of intra-parenchymal ICP monitor** **5) Access for some stereotactic neurosurgery**, including brain biopsy for tumour pathology

Answer 105

Principles of burr hole placement: i) away from major venous sinuses ii) away from air sinuses iii) not overlying eloquent brain. _The following are common sites for placement:_ * *1) Frontal** - midpupillary line - 1 inch behind anterior hair line - to avoid the primary motor cortex * *2) Parietal** - overlying the parietal eminence * *3) Temporal** - 1 inch anterior and superior to external auditory meatus - commonly used in the case of an acute extradural haematoma **4) Occipital**

Answer 106

Classical technique being: 1) Position patient on horseshoe head cushion 2) Check side on CT, which must be displayed in theatre 3) Shave scalp and prepare it with alcohol solution 4) Prepare skin and drape having marked midline and incision. Drape as if for a craniotomy. Plan incision so that trauma flap could be raised if necessary. 5) Incision down to bone approximately 4 cm in length 6) Use periosteal elevator to scrape back periosteum 7) Insert small self-retaining retractor – this should stop all skin edge and galeal bleeding 8) Use the **perforator attached to a Hudson brace** to perforate the outer table of the skull. Continue using the instrument until the inner table has just been perforated and a small amount of shiny dura can be seen. A conical hole should be the result (in the case of an extradural, at this stage dark clot and altered blood should be expressed) 9) Swap the perforator for the burr and widen the hole to its base without damaging the underlying dura 10) If subdural access is needed, score the dura with a no. 15 blade and pick up with a dural hook. Cut onto the dural hook to fashion a cruciate opening of the dura 11) Use monopolar diathermy to coagulate dural leaves 12) Closure: 2/0 Vicryl to galea and clips or 3/0 nylon to skin.

Answer 107

* *1) Bleeding** - Extradural bleeding - Scalp bleeding * *2) Infection** - ventriculitis - subdural empyema - wound infection **3) ‘Plunging’ and damage of underlying structures** **4) Venous sinus damage and possible air embolism** **5) CSF leak** possible if dura opened.

Answer 108

* *Presentation PE:** 1) "Worst headache of my life" 2) Sudden, transient loss of consciousness 3) Vomiting (common). 4) Meningism (nuchal rigidity, photophobia, Kernig) 5) Retinal hemorrhages * *Ix:** 1) CT shows blood in basal cistern (star of David sign) 2) LP showing Xanthochromia (yellow color from RBC lysis); sometimes blood in CSF 3) Cerebral angiogram (DSA CTA MRA) confirming

Answer 109

_Symptoms:_ * *1) Thunderclap headache** - sudden severe * *2) Altered consciousness level 3) Meningism** - neck stiffness - photophibia, phonophobia _Signs:_ 1) Decreased GCS 2) Neck stiffness, Kernig sign 3) Focal neurological signs

Answer 110

_Most common two causes:_ **1) Traumatic SAH** **2) Ruptured saccular (berry) aneurysms** (associated with PCKD) _Others:_ * *3) AVM 4) Brain tumour bleeding 5) Paramesencephalic SAH** - blood is purely located around the midbrain with unknown origin

Answer 111

Associated with PCKD; found @ bifurcations of Circle of Willis: 1) A Comm artery & Ant cerebral artery 2) P Comm artery & internal carotid artery 3) Bifurcation of MCA

Answer 112

* *1) Routine Bloods** - esp CBC, clotting profile **2) CT Brain, consider CT angiogram** * *3) Lumbar puncture for Xanthochromia** - if CTB negative, but still clinically suspicious - due to breakdown products of Hb in the CSF * *4) Consider a formal catheter digital subtraction angiogram (DSA)** - both diagnostic and therapeutic

Answer 113

* *0) Supportive managment** - if traumatic then ABC, ATLS - admit to acute stroke unit, neurosurgical unit - close monitoring, regular neuro obs **1) Flat bed rest** * *2) Triple H therapy** - hypertension - hypervolemia (3L IVF over 24 hours) - haemodilution * *3) Ca channel blocker (nimodipine)** - 60mg Q4H for 21 days - if aneurysmal SAH, in order to prevent vasospasm **4) Prophylactic anti-convulsants** * *5) Early neurosurgery** if aneurysm bleeding - microsurgical clipping - endovascular coiling - endovascular stenting with Flow-diverters

Answer 114

**1) Re-rupture and re-bleeding** * *2) Vasospasm** (Peaks Day 7-10) - presents with altered neurological and new neurological Sx and signs - causing delayed cerebral ischemia **3) Hydrocephalus** (secondary from blockade by hematoma) **4) Seizure** **5) SIADH**

Answer 115

"SAH" **1) Nimodipine** ^{Sea = fish = nimo} **2) **_A_**ngioplasty & intra-arterial papaverine** * *3) Triple _H_ therapy** - Hypervolemia - Hypertension -\> may require vasopressor to induce SBP \>180 - Hemodilution

Answer 116

* *_World Federation of Neurological Surgeons (NFNS) Grades_** - based on GCS and focal neurological signs 1 = GCS 15, no focal neurological deficits 2 = GCS 13-14, no focal neurological deficits 3 = GCS 13-14, focal neurological deficits 4 = GCS 7-12, yes or no focal neurological deficits 5 = GCS \<7, yes or no focal neurological deficits * *_Fisher Grading_** - based on CT appearance 1: no evidence of SAH 2: \<1mm thick 3: \>1mm thick 4: any thickness, but with IVH or parenchymal extension

Answer 117

**1) Rupture**, causing SAH * *2) Mass effect** - Oculomotor palsy (P Com Aneurysm) - Visual loss (Opthalmic artery aneurysm) **3) Thrombo-embolism**

Answer 118

_The most common causes being:_ * *1) Hypertension & Atherosclerotic disease** - giving rise to Charcot-Couchard aneurysms at smaller terminal arteries _Others:_ 3) Aneurysm 4) AVM 5) Brain tumour bleeding 6) Trauma 7) Coagulopathy 8) Amyloid angiopathy

Answer 119

* *1) Basal ganglia** (66%) - Putamen (dilated pupils) * *2) Pons** (10%) - pinpoint pupils **3) Cerebellum** (10%) 4) Other areas * *- brainstem - thalamus** (poorly reactive pupils) * *- lobar or cortical**

Answer 120

_Meningism indicates menigeal irritation, presentation with:_ 1) Headache 2) Nuchal rigidity 3) Photophobia _DDx:_ * *1) Meningitis 2) Subarachnoid haemorrhage**

Answer 121

* *0) Supportive management, ABC** - admission to acute stroke unit, ABC, etc... - NPO, IV fluid - treat fever, correct hypergly with insulin - Neuro-obs * *1) Management of HTN** - IV calcium channel blockers (eg, nicardipine) and β-blockers (eg, labetalol) * *2) Reversal of coagulopathy** - IV vitamin K1 10mg (if warfarin) - Consider prothrombin complex concentrates (PCC); if not available then give FFP **3) Management of raised ICP if any** _±Neurosurgical Intervention (depends)_ **4) Urgent surgical evacuation** in: * Cerebellar ICH, due to high morbidity from rapid development of brainstem compression * Selected large lobar ICH or temporal lobe ICH **5) Conservative treatment** in: * thalamic or brainstem ICH, due to high mortality with no survival benefit * Most supratentorial ICH, due to no benefit

Answer 122

_Based on locations:_ 1) Leptomeninges: meningitis 2) Brain parenchyma: encephalitis 3) Spinal cord: myelitis 4) Pus inside: Brain abscess, Spinal cord abscess 5) Pus outside: Epidural empyema, subdural empyema

Answer 123

1) Neurons don't regenerate - permanent neurological dysfunction 2) Little space in cranium -\> mass effect & cerebral oedema prominently cause damage & herniation 3) Meninges damage will lead to hydrocephalus 4) Antibiotics penetration against BBB is often low

Answer 124

* *1) CNS infection Symptoms & Signs** - meningism (photophobia, nuchal rigidity, headache) - encephalitis signs (altered consciousness, seizures) - raised ICP (morning headache, nausea & vomiting) - other focal neurological signs e.g. sensory, motor disturbances, seizures * *2) Previous or current symptoms suggestive of other foci of infection** - skin rash (purpuric rash if meningococcal) - URTI & diarrhoea common if meningococcal - pneumonia, sinusitis - infective endocarditis * *3) Past medical history** - any chronic infection esp TB - any immunization - any connective tissue disorders * *4) TOCC** - travel history - occupational risk with pigs -\> strep suis - mosquito bite (Dengue fever, Zika virus, Japanese B encephalitis)

Answer 125

_Blood Investigations:_ * *1) CBC for leukocytosis, ESR 2) LFT, RFT, blood glucose for baseline 3) Clotting profile** to guide LP * *4) Blood culture x2** - for smear & culture, viral serology, PCR - before initiating antibiotics (start antibiotics ± dexamethasone after taking blood) _CNS investigations:_ * *4) CT head** to r/o mass effect, note hydrocephalus * *5) Lumbar puncture** - for CSF gram smear and culture, antigen detection - CSF analysis - note opening pressure **6) EEG** if seizure _Septic workup:_ * *7) CXR, Echocardiogram, ENT exam 8) Skull X-ray, sinus, mastoid**if suspect mastoiditis etc. * *9) Sputum, NPA, throat swab, urine, stool** for culture & viral studies

Answer 126

_1) Pyogenic Meningitis_ * *- Neisseia meningitidis - Streptococcus pneumoniae (esp in elderly)** - (Strep suis if pigs) - (E coli, GBS, HI in neonates) - (HI, NM, SP in children) _2) Chronic Meningitis_ * *- Tuberculosis - Cryptococcal neoformans**

Answer 127

* *1) Local transmissino from nearby structures** - nasopharyngeal infection, middle ear, sinusitis - osteomyelitis * *2) Penetrating wound** - Direct spread via skull or meningeal defect (e.g. open skull fracture) - Iatrogenic post-neurosurgery * *3) Hematogenous spread in septicemia** - e.g. IE, lung abscess, pneumonia

Answer 128

_Acute or insidious onset of:_ * *1) Fever, chills & rigor 2) Headache, N+V+ 3) Meningism: Photophobia,****Nuchal rigidity 4) Confusion, decrease GCS 5) Focal neurological deficits** * *±) If Meningococcal** - purpuric rash - prodrome of URTI, diarrhoea * *±) If Streptococcal Suis** - pig and pork product contact - early permanent deafness from cochlear damage

Answer 129

* *1) General Examination** - fever - purpuric rash? * *2) Neurological exam** - focal neurological signs as Cx of meningitis * *3) Meningism signs** (See pic) - Kernig sign: cannot full passive extension of knee when hip knee flexed 90-90 - Brudzinski sign: passive neck flexion will cause hip knee flexion * *4) Fundoscopy** - for papilloedema in case of raised ICP

Answer 130

Mainly in pyogenic and chronic meningitis: * *1) Basal meningeal adhesions** (esp in TB), causing: - obliterate subarachnoid space thus **hydrocephalus, raised ICP** * *2) Cranial nerve palsy** due to entrapment by fibrosis - usu CN 3, 4, 6 (EOM nerves) - CN 8 damage tends to persist **3) Cerebral infarct & stroke** due to thrombosis **4) Seizure** **5) Complicates into cerebritis, cerebral abscess, subdural effusion, empyema** **6) SIADH** _if meningococcemia_ * *7) Spetic shock, DIC 8) Adrenal haemorrhage** (Friederichsen Waterhouse syndrome)

Answer 131

**1) Mycobacterium tuberculosis** **2) Cryptococcus neoformans** - high in pigeon faeces - usually patients are immuno compromised \_\_\_\_\_\_\_ *_less common:_ 3) Treponema pallidum (syphilis)* * 4) Lyme's disease - ticks* * 5) Candida*

Answer 132

0) LP for CSF gram smear & culture, antigen detection - after exclusion of SOL by CT/MRI **1) Empirical Antibiotics ASAP (IV, high dose, good BBB pentration)** - IV Ceftriaxone + IV Vancomycin 📘 ± Ampicillin if anticipate Listeria (pregnant, elderly, immunocompromised) * *±2) adjunctive** **dexamethasone** - before/with first dose of antibiotics to decrease inflammatory complications - if suspect pneumococcal **±3) elevation of head** by 30 degrees and **anticonvulsant** for ICP symptoms relief

Answer 133

All good BBB penetration: * *1) Ceftriaxone** - covers most meningitis bugs except Listeria * *2) Vancomycin** - covers cephalosporin resistant streptococcus * *±3) Ampicillin** - covers Listeria - added if high risk e.g. pregnancy, elderly

Answer 134

1) Chemoprophylaxis with rifampicin before HIB or Neisseria meningitidis contact (Not for pregnant mothers however) 2) active immunisation eg HIB vaccination, meningococcus vaccination, pneumococcal vaccination

Answer 135

Usually presented over days/weeks as a cerebral mass lesion with little evidence of infection: **1) Raised ICP** **2) Seizures** **3) Focal neurological signs** Thus may be difficult to distinguish from cerebral mass lesion e.g. tumour

Answer 136

**1) Local extension** * Frontal lobe from: - paranasal sinus, mastoid, teeth - Strep viridans, anaerobes * Temporal lobe, cerebellum from: - middle ear, sphenoid sinus, mastoid - Strep, pseudomonas, enterobacteriaceae * Cavernous sinus * Orbit * *2) Direct from penetrating wound** - open skull fracture, iatrogenic after surgery * *3) Haematological from distant focus** - e.g. infective endocarditis

Answer 137

NEVER. As brain abscess is a SOL, therefore LP is contra-indicated

Answer 138

* *1) Empirical Antibiotics (IV, at least 6 weeks)** - Pencillin G - Cefotaxime - Metronidazole **2) Steroid** **3) Anti-epileptic prophylaxis** * *4) Clinical radiological monitoring** - serial CT head to monitor progress * *5) Consider surgical drainage** - stereotactic/US guided aspiration - craniotomy and excision of abscess cavity

Answer 139

• Skin • Subcutaneous tissue • Fat • Supraspinous ligament • Interspinous ligament • Ligamentum flavum • Epidural fat • Dura mater • Arachnoid mater -\> into subarachnoid space

Answer 140

1) Left lateral postion, back & knees flexed 2) Aseptic technique 3) Inject LA to skin _4) Insert LP needle at cranial angle of 10-20 degrees at:_ - **between spinous processes of L3/4, L4/5, or L5/S1 - i.e. below the level at which the spinal cord ends (L1 in an adult, but lower in a child as a result of differential growth** 5) ‘Pop’ is often felt as the ligamentum flavum is traversed 6) Remove stylet to allow CSF to drip out (do not aspirate) 7) Note appearance & measure opening pressure 8) Remove spinal needle 9) Patient should remain flat for at least 30 min to prevent a low pressure headache.

Answer 141

* *1) Raised ICP & space occupying lesion** - based on CT (unequal pressures between supra- and infra-tentorial compartments) - clinical signs of papilloedema, false localising signs **2) Bleeding tendency** **3) Local infection @ area of needle insertion** **±4) Local anatomical disturbance** e.g. severe kyphoscoliosis

Answer 142

_Lumbar puncture may cause:_ **1) headache** **2) dry tap** **3) subdural hematoma** **4) aneurysmal subarachnoid hemorrhage** * *5) brain herniation** - if SOL exists in the brain

Answer 143

Brain tumours can be classified into: _A. Brain metastasis (most common)_ _B. Primary Intrinsic tumours (i.e. Neuroectodermal tumour)_ * *1) Glioma** - astrocytoma, glioblastoma multiforme * *2) Tumours from Neurons and primitive cells** - neuroblastoma, medulloblastoma _C. Extrinsic tumours_ **1) Meningioma** **2) Pituitary tumour** **3) Vestibular Schwannoma**

Answer 144

**1) Lung (40%)** **2) Breast (20%)** **3) Malignant Melanoma (10%)** 4) Genitourinary (esp Kidney) 5) Gastrointestinal

Answer 145

Depends on the grading: _Low grade_ I - pilocytic astrocytoma II - astrocytoma * diffuse, slow growing * resection can be curative _High grade_ III - anaplastic astrocytoma IV - glioblastoma multiforme * Rapidly growing, high malignancy * Very poor prognosis

Answer 146

* *1) Supportive medical treatment** - Dexamethasone to decrease cerebral oedema - Anticonvulsants **2) Biopsy** *Definitive plan depends on grading:* _if low grade_ **3) Surgical craniotomy** for curative resection _if high grade_ **3) Maximal safe resection** if possible, consider surgical debulking * *4) Chemo-RT** - tele-radiotherapy - oral temozolomide **5) Anti-angiogenesis agents** e.g. bevacizumab * *6) Rehabilitation** - PT, OT, speech - clin psy

Answer 147

_Meningioma:_ - slow growing, benign tumour; may undergo malignant change in 1-2% - arises from arachnoid granulations - causes reactive hyperostosis and may invade adjacent bone

Answer 148

* *1) Skull radiograph:** - boney hyperostosis with sunray effect and calcification * *2) CT** - well demarcated homogenous lesion - may be calcified with surrounding oedema * *3) MRI** - Iso-intense on T1W image - striking enhancement with gadolinium contrast * *4) Angiogram** - very vascular lesions

Answer 149

**1) Corticosteroid** **2) Anti-epileptics** * *3) Surgical resection** - with the aim of complete resection of tumour and the meningeal origin - recurrence depends on the completeness of tumour resection

Answer 150

Schwannoma of CN VIII, might be part of NF2 esp if bilateral * *Clinical Feature:** - unilateral progressive sensorineural hearing loss - vertigo and tinnitus is rare (due to slow growth, thus allows compensation) - hydrocephalus from obstruction of 4th ventricle **Ix:** MRI _Management:_ * *1) Conservative management** w/ serial imaging - if small and asymptomatic, as it is a slow growing tumour * *2) Surgical excision 3) Stereostatic radiosurgery**

Answer 151

* *1) Schwannoma** - "acoustic neuroma" - other CN (not I or II) schwannoma - spinal schwannoma - peripheral nerve schwannoma * *2) Other nervous system tumours** - meningiomas - ependymomas - astrocytoma * *3) Eye signs** - Cataract (early onset) - Retinal harmatoma - Optic nerve meningioma * *4) Very little Skin involvement** - less than 6 cafe au lait spots - cutaneous schwannomas (plaque lesions)

Answer 152

**1) Pituitary adenoma** (in adults) **2) Pituitary Carcinoma** (very rare; secondary more common than primary tumour) (in children: **craniopharyngioma**, **CNS germ cell tumour**)

Answer 153

* *Based on Endocrinology** - functional (secreting, ~80%) - non-functional (non-secreting) * *Based on Size:** - Microadenomas \< 10 mm (observe if non-secreting) - Macroadenomas \> 10 mm (surgery mostly) - -------------------------- * *Functional putuitary adenoma:** - Prolactinoma (most common) - GH producing tumour - ACTH producing tumour - Glycoprotein secreting tumours (TSH, FSH, LH, α, β- subunits)

Answer 154

* *1) Local symptoms** - visual loss (bitemporal hemianopia from optic chiasm) - hydrocephalus (3rd ventricle), raised ICP Sx 2a) Usually **hypopituitarism** from mass effect * GH: growth retardation, central obesity, round face * FSH, LH: hypogonadism, infertility, amenorrhoea * ACTH: adrenal insufficiency e.g. weight loss, orthostatic hypotension, hypoglycemia, hyponatremia, but NO hyperpigmentation like Addison's) * TSH: hypothyroidism 2b) Symptoms of **pituitary hormone hyper-secretion** if functional adenoma: * Prolactin: galactorrhoea, amenorrhoea, impotence * GH: gigantism in children, acromegaly in adult * ACTH: Cushing's disease * TSH: rarely, 2º hyperthyroidism 3) Incidental **radiological finding** on skull X-ray, CT scan or MRI

Answer 155

* *_1) Radiology_** - MRI (preferred) - CT (better visualisation of calcification) **_2) Blood test_** for screening of functional pituitary adenoma (which might be asymptomatic): a) Prolactinoma - increased serum prolactin (\>10x increase, beware of false negative hook effect) - 50%+ size shrinkage with dopamine agonist b) GH-producing tumour - serum GH or IGF1 (insulin like growth factor) increased (difficult coz short t_1/2) - Stimulation test with Insulin tolerance test or arginine infusion test - Supression test e.g. OGTT showing non-suppressible serum GH

Answer 156

* *1) Medical therapy for secreting pituitary adenoma** a) Prolactinoma - dopamine agonists i.e. bromocriptine, carbegoline - first line b) GH/TSH secreting tumour - somatostatin analogues e.g. Octreotide, Lanreotide - adjunct to surgery & RT * *2) Surgical resection** (usu trans-sphenoidal) - for macroadenoma - for secreting tumour (e.g. ACTH, GH) - when medical therapy for prolactinoma failed * *3) Radiotherapy** (tele-radiotherapy or radiosurgery e.g. Gamma knife, X-knife) - if unfit for surgery - Macroadenoma, esp macroprolactinoma - as adjunct, esp in persistent hormonal hyperfunction despite surgical intervention

Answer 157

**1) Transphenoidal** -\> route of choice **2) Transfrontal** -\> for very large suprasellar extension, esp with severe chiasmal compression

Answer 158

1) Mortality – very rare 2) Endocrine - diabetes insipidus, hypopituitarism 3) Visual loss 4) CSF leakage & meningitis 5) Vascular injury & CVA 6) ENT symptoms 7) Intracranial haemorrhages etc

Answer 159

Hemorrhagic infarction of pituitary tumour * *Presentation:** - Variable onset of severe headache - Meningism - Vertigo - Visual defects e.g. bitemporal hemianopia - Altered consciousness

Neurosurgery Flashcards

(183 cards)