Scenarios Flashcards
What are the main causes of a mass in the posterior fossa of an adult?
Met Met Met
What is the differential diagnosis of a posterior fossa mass in an adult?
A - Tumour 1) Metastasis 2) Haemangioblastoma (10%) - mural nodule with cyst. Look for flow voids 3) Pilocytic astrocytoma - young adults 4) Brainstem glioma 5) Choroid plexus tumour 6) Cerebellar liponeurocytoma B - Infection (Abscess) C - Vascular (cavernoma / haemorrhage / infarct)
What are the radiological features of Lhermitte-Duclos?
Tiger stripes with widening of the folia. Non-enhancing. Can be focal or diffuse.
What is the DD of multiple posterior fossa lesions?
1) Metastases 2) Abscess 3) Haemangioblastoma (think VHL!) 4) Cavernomas
What proportion of paediatric tumours are in the posterior fossa?
2/3
What is the differential diagnosis of a posterior fossa tumour in a child?
1) PNET incl Medulloblastoma 2) Pilocytic astrocytoma 3) Brainstem glioma 4) Ependymoms 5) Choroid plexus papilloma 6) ATRT 7) Mets (neuroblastoma / rhabdomyosarcoma / Wilms)
What is the most common location for a medulloblastoma?
Roof of the 4th ventricle (fastigium)
How can medulloblastomas be differentiated from ependymomas?
1) Medulloblastomas may show the ‘banana sign’ where there is a cleft of csf between the lesion and the floor of the 4th V. 2) Medulloblastomas are haemogenous 3) Calcification more common with ependymomas 4) Ependymomas grow out of the foramen of lushka
What are the molecular subtypes of medulloblastoma?
1) Wnt (10%) - usually in the cerebellar peduncle. Associated with a mutation in the b-catenin gene. Best prognosis. 2) SHH (20%) - usually in the cerebellar hemisphere. Intermediate prognosis. Associated with mutations in PTCH, SUFU, GLI1 and GLI2. 3) Group 3 (30%) - Midline with prominant enhancement. MYC amplification; GABAergic expression. 4) Group 4 (40%) - Midline with little enhancement. CDK6 and MYCN mutations. Glutamatergic expression.
What is the most common location for a pilocytic astrocytoma in a child?
Cerebellar hemisphere
Where do ependymomas arise from?
Floor of the 4th ventricle
What is the DD of a CP angle lesion?
Vestibular schwannoma Meningioma Epidermoid Metastasis Trigeminal / facial schwannoma Arachnoid cyst Neurenteric cyst Aneurysm Extension of glioma Cholesterol granuloma
What are the causes of a cystic lesion in the CP angle?
Arachnoid cyst Epidermoid cyst (restricted DWI) Dermoid cyst (high T1 and midline) Cystic schwannoma Neurenteric cyst
What is the classical presentation of a vestibular schwannoma?
Progressive unilateral hearing loss with tinnitus Vertigo is rare CN5 involvement does not occur unless >3cm - check the corneal reflex! Facial nerve involvement suggests a meningioma
Where do CP angle meningiomas arise from?
The superior anterior edge of the IAC Facial nerve palsy before hearing loss and more commonly have trigeminal neuralgia
What lesions affect the petrous apex?
Gragenigo’s syndrome Cholesterol granuloma Aneurysm SCC Glomus tumour Chondrosarcoma
What is the differential diagnosis of a foramen magnum lesion?
Meningioma Chordoma Epidermoid Chondrosarcoma Metastasis Exophytic lesion arising from the brainstem
What is the DD of white matter lesions?
1) Ischaemia (small vessel) 2) Demyelination 3) Vitamin def 4) Viral (PML/ HSV. HIV/CMV) 5) Metabolic derangements (CPM) 6) Low grade glioma
What is the DD of a lesion in the corpus callosum?
Butterfly GBM
Lymphoma
MS
Tumefactive demyelination
Lipoma
DAI
What is the DD of a pituitary tumour?
Adenoma / Carcinoma Craniopharyngioma Rathke cleft cyst Germ Cell Tumour Metastasis Aneurysm Astrocytoma Hypothalamic glioma Optic nerve sheath tumour Epidermoid cyst Chordoma Arachnoid cyst Pseudotumour i.e. physiological enlargement in puberty / pregnancy
What are the classical MR spectroscopy features of a low grade tumour?
Choline - Cr - NAA peaks form a 45 degree angle (Hunter’s angle)
What is the triad of clinical features associated with a suprasellar GCT?
DI, Panhypopituitarism and visual deficit
Lesion in the pineal and pituitary region. What is the diagnosis?
Synchronous GCT
What are the two types of hypophysitis?
Lymphocytic (late pregnancy / post partum) and granulomatous
How can hypophysitis be distinguished from a pituitary adenoma?
Hypophysitis has dilation of the pituitary stalk, symmetric pituitary enlargement, intense enhancement and loss of the posterior pituitary bright spot.
What is the difference between Schizencephaly and Porencephaly?
Schizencephaly is lined by grey matter (can be open or closed lip) whilst porencephaly is not lined by grey matter
What is the term given to when there is separation of the fornix and the roof of the 3rd ventricle?
Cavum velum interpositum
What is the difference between a cavum septum pellucidum and cavum septum vergae?
The CSP is anterior to the columns of the fornix whilst the CSV is posterior to the columns of the fornix
What is the differential diagnosis of a cavernous sinus lesion?
Meningioma Neurinoma Metastasis Pituitary tumour Lymphoma Aneuryms CCF Chordoma
What is Tolosa-Hunt syndrome?
Inflammation affected the superior orbital fissure / Cavernous sinue causing painful opthalmoplegia
What is the differential diagnosis of an intraventricular tumour?
Astrocytoma Colloid cyst Craniopharyngioma SEGA Meningioma Ependymoma / Subependymoma Craniopharyngioma Medulloblastoma (4th vent) Choroid plexus papilloma Central neurocytoma
What is the differential diagnosis of diffuse meningeal thickening / enhancement?
Intracranial hypotension Meningitis Carcinomatosis Metastasis Sarcoid / TB
What condition causes injury to the caudate and putamen?
Hypoglycaemia
What condition causes atrophy of the caudate only?
Huntingtons chorea
Describe the imaging findings.
The T2W reveals lesions in the right cavernous sinus and CPAs bilaterally.
The cavernous sinus lesion appears to be extending from Meckel’s cave and may represent a trigeminal schwannoma or meningioma.
The T1W contrast image reveals nodular enhancement of the left cisternal CN5 as well as the right cavernous sinus lesion and left VS.
The findings would be in keeping with NF2 in which schwannomas, multiple meningiomas and ependymomas are associated.
Describe the imaging findings.
The T1W contrast enhanced image reveals a large right CPA lesion extending into and widening the IAM (Trumpet sign). There is significant brainstem compression with mass effect on the right middle cerebellar peduncle and cerebellar hemisphere. The 4th venticle appears displaced and effaced but remains patent.
The hypointense non-enhancing component in centre represents an intramural cyst.
Describe the image.
The coronal T2 image centred on the right IAM shows a lesion superior to the falciform (horizontal crest), which most likely represents a Koos 1 vestibular schwannoma of the superior division of the vestibular nerve. A loop of the AICA can also be seen entering the meatus.
Describe the image.
Axial GRE sequence showing a blooming artefact within a large right CP angle lesion indicative of microhemorrhages within a vestibular schwannoma. The differential would be calcification within a meningioma.
Describe the image.
T1 and T1 contrast-enhanced images of a right CPA reveal vestibular schwannoma extending into the right IAM. There is peripheral enhancement. The central region returns high T1 signal indicating intramural cystic change due to haemorrhage.
Describe the image.
Diffusely contrast-enhancing lesion overlying the left IAM with a dural tail extending along the petrous dura. There are flow voids extending radially in a fan shape distribution representing the dural blood supply to the core. The features suggest a CP angle meningioma. The differential includes a vestibular schwannoma, dural metastasis, epidermoid cyst or inflammatory pseudotumour.
Describe the image.
Coronal T1 with contrast reveals a large contrast-enhancing lesion extending from the tentorium to the level of C1. There is invasion of the IAM, middle ear, jugular foramen and foramen magnum. These findings would be indicative of a meningioma as there appears to be a tentorial dural tail. It would be important to understand how ventral the lesion extends and its relationship to the vertebral artery,
What is the dural blood supply to the posterior fossa meninges?
Vertebral arteries
Occipital arteries
Ascending pharyngeal arteries
Note supply to the tentorium is via the meningohypophyseal trunk, posterior meningeal artery (from the Ascending pharyngeal and vertebral arteries) and the artery of Davidoff and Schecher.
Describe the image.
Coronal contrast T1 reveals a lesion in the right CPA causing mass effect on the adjacent brainstem. There is normal contrast enhancement of the contralateral choroid plexus. There does not appear to be any leptomeningeal enhancement.
Axial FLAIR reveals a substantial vasogenic edema in the right brachium pontis and deep cerebellar nuclei. The left flocculus is normal.
Where is the cochlear nucleus?
In the lateral inferior cerebellar peduncle (blue arrow). i.e. anterior border of foramen of Luschka
What hypodense lesions are found in the CPA?
Lipomas (bright on T1 and T2 and dark on fat-saturated sequences. Chemical shift artefact)
Arachnoid cysts - follows CSF no restricted diffusion
Epidermoids - follows CSF with restricted diffusion
Neuroenteric cysts - bright on T1 due to proteinaceous content and does not fat-saturate
Describe the image.
CT scan reveals a hypodense lesion at the fundus of the right IAM. The Hounsfield units appear lower than that of CSF in the 4th ventricle but not as low as air suggesting that is a lipoma. The T1 image reveals high signal intensity confirming this is a CP angle lipoma. Fat saturated images would be helpful. The differential would be an epidermoid or haemorrhage into an arachnoid cyst.
Describe the image.
CT - low-density lesion in the left CPA.
FLAIR - incomplete fluid attenuation. The surrounding region of increased FLAIR signal in the cerebellum indicates gliosis within the cerebellar hemisphere.
DWI - restricted diffusion.
These findings are suggestive of an epidermoid cyst. The differential includes neurenteric cyst (would be bright on T1 due to proteinaceous fluid content).
What are the histological features of an epidermoid?
Macro - pearly white mass with lobulated / cauliflower appearance. Filled with soft creamy/waxy material.
Micro - Cyst wall is stratified squamous epithelium with a fibrous capsule. Cyst contains keratin and cholesterol-rich fluid. No dermal derived tissue (skin / hair follicles) otherwise would be a dermoid!
Describe the image.
T1W contrast enhanced image reveals a lesion in the right CPA. This does not show contrast enhancement. The lesion has irregular borders and extends through and expands the foramen of Luschka.
The T2W image reveals high signal. I would expect a FLAIR image to show incomplete fluid suppression and a diffusion-weighted image to show restriction in keeping with an epidermoid.
What causes arachnoid cysts to form?
Congenital splitting of the arachnoid resulting in a CSF filled cavity. These follow CSF on all sequence, have no contrast enhancement and do not show restricted diffusion. The differential is an arachnoid cyst, neurenteric cyst or cystic neoplasm e.g. cystic vestibular schwannoma / cystic meningioma.
What is a Bell’s palsy?
An idiopathic facial nerve palsy thought to be due to reactivation of HSV in the geniculate ganglion.
Describe the imaging in this patient with right trigeminal neuralgia
T2 sequence of revealing a hyperintense region in the lateral pons at the exit of the trigemimal nerve. There is no vascular conflict visible. The findings would be suggestive of MS or a focal brainstem tumour as the cause of the TN. Further imaging of the brain and CSF examination would be warranted.
Describe the image in this patient with hemifacial spasm.
MRA reveals an ectatic vertebral artery with a PICA branch in contact with the root entry zone of the CN7.
Axial CISS confirms vascular conflict with the CN7/8 complex and displacement posteriorly causing kinking at the posterior margin of the porus.
What are the treatment options for hemifacial spasm?
Conservative
Medical with botox injections (needs repeating every 4 months)
Surgical with MVD of the facial nerve.
How does the patients age affect the differential diagnosis of a pituitary lesion?
Children are more likely to have craniopharyngiomas and pilocytic astrocytomas of the hypothalamus / optic pathway.
Adults are more likely to have pituitary adenomas, meningiomas and aneurysms.
What are the causes of pituitary hyperplasia?
- Physiological - puberty / pregnancy
- End organ dysfunction (primary hypothyroidism / adrenal dysfunction etc)
- Intracranial hypotension and dAVFs due to venous engorgement
What are the causes of pituitary gland infiltration?
Inflammatory (lymphocytic / granulomatous) hypophysitis
Neurosarcoidosis
Lymphoma
TB
Metastasis
What is the cause of a suprasellar mass in a child?
- Craniopharyngioma
- Pilocytic astrocytoma of the hypothalamus / optic pathway
- Germinoma (F>M)
- Histiocytosis
What is the cause of a suprasellar mass in an adult?
Pituitary macroadenoma
Meningioma
Aneurysm
Craniopharyngioma (papillary subtype)
Rathke’s cleft cyst
Metastasis
What is the 90% rule with craniopharyngiomas?
90% calcified
90% cystic
90% enhance
Describe the anatomical structures in this pituitary region
Non-contrast T1 shows normal posterior pituitary bright spot in 80%. This does not suppress with fat saturation. Contrast administration shows diffuse enhancement of the anterior and posterior pituitary, infundibulum and tuber cenereum.
The diaphragma sella forms the roof of the sella and that this point the arachnoid does not continue into the sella so this pituitary gland is not surrounded by CSF.
Describe the image.
Sagittal T1 contrast image shows a complex heterogenous sellar and suprasellar lesion with both solid and cystic components. The floor of the third ventricle is elevated and optic chiasm is displaced and not discernible. There is no synchronous lesion in the pineal region.
These features are in keeping with an adamatinomatous craniopharyngioma.
Describe the image.
Coronal T1 with contrast reveal a complex sellar and suprasellar lesion with extension laterally through the right choroidal fissure resulting in mass effect and displacement of the right basal ganglia. The hyperintense region at the lateral margin is indicative of haemorrhage. These findings in an adult are in keeping with a macroadenoma.
What is the diagnosis?
Ectopic posterior pituitary. Located at the floor of the third ventricle in the median eminence of the hypothalamus.
What are the features of hypothalamic dysfunction?
Hyperphagia>morbid obesity
Temperature dysregulation
Sleep-wake cycle disturbance
DI
Hyperproloactinaemia
Precocious puberty
Rage attacks
What is the diagnosis?
Septo-optic dysplasia.
The optic chiasm is extremely thin.
The posterior pituitary bright spot is at the median eminance in the floor of the third ventricle.
There is no infundibulum or anteiror pituitary gland visible.
Due to the absence of the septum pelludicum the fornix is very low lying.
What is the diagnosis?
Hypothalamic hamartoma (pedunculated subtype). The lesion is midway between the infundibulum and the mammillary bodies and is isointense to grey matter. Presentation is with hypothalamic dysfunction (hyperphagia, temperature dysregulation, altered sleep-wake cycles, rage attacks, DI, endocrinopathy), precocious puberty and gelastic seizures.
The differential is an ectopic posterior pituitary, craniopharyngioma, germinoma and hypothalamic pilocytic astrocytoma / opg.
What is the diagnosis?
Sessile HH.
The lesion is in the floor of the third ventricle with appearances of grey matter on both T2 and FLAIR sequences arising from the lateral wall of the inferior third ventricle. This would not enhance with contrast.#
Hypothalamic hamartomas are associated with Pallister-Hall syndrome.
What is this sellar / suprasellar lesion?
The appearances are that of a Rathke’s cleft cyst.
The CT does not reveal any calcification allowing distinction from a craniopharyngioma.
These are non-enhancing and are situated between the anterior and posterior pituitary (in the pars intermedius).
There is elevation of the optic chiasm.
What is the success of medical therapy for prolactinomas?
80-90%
What is dynamic contrast-enhanced MRI for pituitary lesions?
T1 coronal MRI taken at 5-second intervals after bolus contrast administration.
Thin coronal slices with no gap.
May reveal a filling defect with microadenomas as these enhance slower than the surrounding normal pituitary gland.
Where are prolactin and ACTH (Cushing’s) adenomas usually located?
Prolactin = peripheral
Cushings = central
What is the classical radiological appearance of a macroadenoma?
Snowman. There is elevation of the chiasm.
What is the diagnosis?
Large sella and suprasellar mass with invasion of the right cavernous sinus reaching the lateral border and circumferential encasement of the right carotid artery = Knosp grade 4.
If this is not a prolactinoma and surgery is performed then the sellar and suprasellar components can be resected but the cavernous sinus portion should be left and given SRS (20 Gy for non-functional and 25 Gy for functional).
The differential diagnosis includes craniopharyngioma, meningioma, germ cell tumour, hypothalamic pilocytic / OPG, metastasis and aneurysm.
Describe the imaging.
T1 sagittal image revealing a sellar and suprasellar lesion with erosion of the clivus and extension into the nasopharynx. There is invasion of the third ventricle which appears occluded. The lesion is heterogenous with regions of mural cystic degeneration. The posterior pituitary bright spot can be seen.
What is the diagnosis?
T1 midline sagittal section through the pituitary fossa revealing a sellar lesion expanding the sphenoid sinus extending into the sphenoid sinus. The thick skull and enlarged frontal sinuses are indicative of macroadenoma associated with acromegaly.
The differential of a macroadenoma includes apoplexy, craniopharyngioma, chordoma, meningioma and metastasis.
What is suggested by sudden onset headache, ophthalmoplegia and endocrinopathy?
Pituitary apoplexy - usually into a preexisting macroadenoma
Describe the image?
T2 coronal reveals a complex sellar and suprasellar heterogenous mass extending into the third ventricle and right cavernous sinus.
The sagittal contrast T1 image shows a fluid level anteriorly. There is patchy enhancement suggestive of necrosis in the non-enhancing components.
This is pituitary apoplexy into a macroadenoma. The differential diagnosis includes craniopharyngioma, macroadenoma, RCC, giant sellar aneurysm and germinoma.
Treatment includes steroids, urgent endocrine assessment, visual field assessment. Early surgical decompression (<7 days) is controversial.
What syndrome is pituitary apoplexy associated with?
HELLP syndrome: Haemolysis, Elevated Liver enzymes, Low Platelets
Sheehan syndrome: Peripartum infarction / haemorrhage into the anterior pituitary
What are risk fx for pituitary apoplexy?
Hypertension
Major surgery e.g. cardiac
Anticoagulation
Head trauma
Pregnancy (Sheehan’s syndrome)
What is the differential or a cerebellar lesion in an adult?
Mets Mets Mets Abscess (look at the mastoids!) Hemangioblastoma GBM Pilocytic astrocytoma / medulloblastoma (young adults) Ependymoma / subependymoma Epidermoid / dermoid Choroid plexus papilloma Cavernoma Stroke Lhermitte-Duclos (dysplastic gangliocytoma)
What is the differential or a cerebellar lesion in a child?
Medulloblastoma Ependymoma Pilocytic astrocytoma Met (Wilms / rhabdomyosarcoma / neuroblastoma) DIPG Choroid plexus papilloma
What is the differential or a CP angle lesion?
Vestibular schwannoma Meningioma Trigeminal / lower cranial nerve schwannoma Met Brainstem glioma Abscess Epidermoid Aneurysm Glomus tumour Chordoma Neurenteric cyst
How do you differentiate a vestibular schwannoma from a meningioma?
VS present with progressive unilateral SN hearing loss, facial nerve weakness is late. Loss of corneal reflex when >3 cm. Heterogenous enhancement. IAC becomes enlarged. Not calcified. Meningiomas arise from the superior edge of the IAC and cause early facial nerve weakness. Hearing loss is late. Trigeminal neuralgia is more common. Homogenous enhancement. IAC not enlarged. Calcify.
Differential of a petrous apex lesion?
Gradenigo’ syndrome Cholesterol granuloma SCC Glomus tumour Chrondrosarcoma (displaces the carotid laterally)
Differential of a foramen magnum lesion?
Meningioma Chordoma Chrondrosarcoma Met Epidermoid Pannus Exophytic brainstem tumour
What is a rotating paralysis?
Seen with FM lesions. Weakness affects the ipsi UL > ipsil LL > contra LL > contra UL
What type of nystagmus occurs with FM lesions?
Classically down beat
How do you differentiate a GBM from an abscess?
Clinical condition of the patient (fever/WCC/CRP etc) Ring enhancement is complete and thick with abscess. Strong restricted diffusion.
What is leukoencephalopathy?
Disease confined to the WM - likely demyelinating lesion (MS / ADEM).
Differential of a corpus callosum lesion?
Lymphoma, MS, ADEM, GBM, lipoma, Diffuse axonal injury
The differential of a sellar lesion?
Adult = pituitary adenoma > craniopharyhngioma , meningoma of tuberculum sella, aneurysm Child = Craniopharyngioma, germinoma, rathke’s cleft cyst > pituitary adenoma. OPG in NF1. Suprasellar arachnoid cysts Other things = Langerhans histiocytosis / lymphocytic hypophysitis *Enlarged pituitary may be physiological (pregnancy / pubertry)
How do you differentiate pituitary adenoma from lymphocytic hypophysitis?
Hypophysitis is common surrounding pregnancy. Symmetrical diffuse thickening of gland and stalk. Intense enhancement. Loss of pituitary bright spot.
What are the types of autoimmune hypophysitis?
Lymphocytic and granulomatous.
Most important clinical feature for lymphocytic type is that it occurs peri-pregnancy
Treat with steroids!
What intracranial cyst do you know?
Arachnoid cysts
Epidermoid cysts
Porencephalic cysts
Schizencephaly
Neuroenteric cysts
Pineal cyst
Colloid cysts
Haemoangioblastoma
Cystic meningiomas
Cystic schwannomas
Infective cysts (neurocysticerosis secondary to taemia solium and hydatid cyst secondary to echinococcus)
How do you differentiate cavum septum, cavum vergae and cavum velum interpositum?
Cavum septum is anterior to foramen of monroe between the leaflets of septum pellucidum.
Cavum vergae is posterior to foramen of monroe. Associated with Apert’s syndrome!
Cavum velum interpositum extends below the splenium and above the roof of the 3rd ventricle / internal cerebral veins. It is due to separation of the crura of the fornix and the thalamus.
What is the differential of an orbital lesion?
Pseudotumour (most common intraconal lesion)
Meningioma
OPG
Optic nerve schwannoma
Cavernoma
CCF/AVM
Melanoma
Retinoblastoma
Lymphoma
Grave’s disease
Fibrous dysplasia
Dermoid (in a child)
What is the differential of a cavernous sinus lesion?
Meningioma
Schwannoma
Pituitary adenoma
Chordoma
Metastasis
Lymphoma
Mucocele
Tolosa Hunt syndrome
Cavernous sinus aneurysm / fistula / thrombosis
What are the causes of leukoencephalopathy?
Demyelination (MS/ADEM)
Infections (PML/HSV/CMV)
Hyponatraemia
Metachromic leukodystrophy
Toxins (Carbon monoxide/ cyanide etc)
Vitamin def (B12)
Low grade glioma
How do you categorise orbital tumours?
Ocular / Optic nerve / Intraconal / Extraconal
What is the most common orbital lesion?
Orbital cavernous haemangioma (cavernoma)
Displaces the optic nerve and rectus muscles (intraconal)
Well defined
Bright on T2
Progressive filling enhancement pattern
Treatment is conservative unless they grow or are symptomatic and then surgical removal is curative
Differential is a schwannoma / meningioma / melanoma / lymphoma
What is the main difference between a capillary haemangioma and a lymphangioma?
Both causes infantile proptosis. Capillary haemangiomas regress spontaneously whilst lymphangiomas do not! Lymphangiomas get worse with URTIs. MRI of a lymphangioma is shown.
What is this?
Capillary haemangioma
What is this?
Dilated opthalmic artery (white arrow heads) seen filling into dural AVF (black arrow). Dilated venous varices (white arrows) seen in later phase.
What is this condition?
Wyburn-Mason syndrome.
Telangiectasia on the face. AV extending from the orbit along the optic pathway to the midbrain with large varix draining into the superior petrosal sinus.
What is this?
A CCF with an arterialised superior ophthalmic vein
What is an orbital pseudotumour?
The most common orbital lesion in adults.
Idiopathic inflammatory lesion of the orbit that involves the extraocular muscles (most commonly the lateral rectus)
Rule out Grave’s disease!
What is leontiasis ossea?
Fibrous dysplasia of the skull and face which makes the patient look like a lion!
Which tumours can have a dural tail?
Meningioma
Pleomorphic xanthroastrocytoma (see picture)
What is the cause of bilateral high T1 signal in the globus pallidus?
Manganese toxicity
What are the most common orbital tumours in a child?
Dermoid 37%
Cavernous Haemangioma 12%
Rhabdomyosarcoma 9%
Optic nerve glioma 6%
Lymphangioma 5% - if bleeds = chocolate cyst!
Retinoblastoma (40% bilateral and 90% calcified)
What is the most common cause of sharply demarcated full-thickness lesions?
Myeloma
Noted: LCHs are often tender so can be distinguished
Patient with cafe au lait spots, precocious puberty and skull lesions. What is the diagnosis?
McCune-Albright syndrome
What are the causes of diffuse skull thickening?
Fibrous dysplasia
Paget’s disease
Osteopetrosis
Thalassaemia and other haematological dyscrasias that cause extramedullary haemopoiesis
Chronic phenytoin use
Hyperostosis frontalis interna
What structures are hyperdense in the brain?
Calcium
Blood
Melanin
Contrast medium
(Foreign body)
What is the differential diagnosis of an intraventricuar tumour?
Mnemonic = MSCENTRAL
Meningioma / Metastasis
SEGA / Subependyma nodule
Choroid plexus papilloma / Colloid cyst / Craniopharyngioma
Epidermoid / Ependymoma / Subependymoma
Neurocytoma
Teratoma / Tuber
Ruptured epidermoid
AVM / Aneurysm / Abscess
Lipoma
What causes leptomeningeal enhancement?
Infections (pyogenic / viral e.g. CMV / TB etc)
Metastasis / carcinomatosis (sugar-coating)
CNS lymphoma (nodular)
Intracranial hypotension
Neurosarcoidosis
What is the most common cause of a thalamic lesion?
Astrocytoma
In children also think diffuse midline glioma (H3 histone M27K) and PNET
Which lesions are intranasal and intracranial?
Infections (sinusitis / mucocele)
Olfactory groove meningioma
Esthesioneuroblastoma
Nasopharyngeal carcinoma / Sinonasal undifferentiated carcinoma
Encephalocele (swells with valsalva = furstenberg’s sign)
What are the causes of atlantoaxial subluxation with increased ADI?
Rheumatoid arthritis (erosion of the entry point of the transverse ligament) Trauma Congenital laxity (Downs / NF) Retropharyngeal infection (Grisel syndrome) Chronic steroid use
What are the causes of atlantoaxial subluxation with normal ADI?
Odontoid fracture Os odontoideum (orthotopic type) Erosion of the odontoid due to Rheumatoid arthritis Neoplastic erosion of the odontoid Morquio syndrome - hypoplasia of the odontoid Transoral / endonasal odontoidectomy
What primary bone tumours affect C2?
Chondroma
Chondrosarcoma
Osteoblastoma
Osteoid osteoma
Osteosarcoma
Chordoma
Giant cell tumour
Aneurysmal bone cyst (see picture)
What are the features of morquio?
Type 4 mucopolysaccharidosis
Short stature
Odontoid hypoplasia resulting in atlanto-axial instability
Platyspondyly of the vertebra (flattened)
Radial hypoplasia / curvature
Short metacarpals
Pectus carinatum
Scoliosis
Oar shaped ribs
Cox valga deformity secondary to dysplastic femoral heads
Which condition causes calcified intervertebral discs?
Ankylosing spondylitis (spares the nucleus pulposus)
What is vertebra plana?
Completely collapsed vertebral body, sparing the discs and neural arches. No kyphosis.
Secondary to LCH, collapsed fracture, TB and haemangiomas
Which conditions cause posterior scalloping of the vertebral bodies?
Mnemonic = AMEN
Acromegaly Achondroplasia
Marfan’s Morquio
Ehlers-Danlos
Neurofibromatosis
**Also think nerve sheath tumours if at the neural foramen
(Note: anterior scalloping is caused by TB and lymphoma!)
Which infection spares the vertebral disc?
TB (also think metastases and multiple myeloma)
What causes presacral teratomas?
Sequestered cells from Hensen’s node in the caudal embyro. May be associated with Curarinho syndrome (sacral dysgenesis, pre-sacral mass and dysraphism)
Where does ankylosing spondylitis effect (by definition)?
The sacroiliac joint (based on the modified New York criteria is sacroilitis + one other feature in a patient with >3 months of back pain and onset <45 years)
What causes sacral agenesis?
Caudal regression syndrome. The associated spinal cord abnormalities are due to failure of secondary neurulation.
What causes diffuse nerve root enhancement in the spinal cord?
Tumours = lymphoma / leptomeningeal carcinomatosis
Infection = CMV, meningitis
Inflammatory = GBS / arachnoiditis / sarcoid (look for hilar lymphadenopathy!)
What causes nodular nerve root enhancement in the spinal cord?
NF
Drop mets
Neurofibroma
Schwannoma
What are the causes of a cystic lesion in the spine?
Meningeal cyst
Arachnoid cyst
Cystic schwannoma
Ependymoma with capping cyst
Syrinx
Dilated central canal
How do you approach a patient with syncope?
Orthostatic vitals ECG / 24 hour tape Review drugs (beta blockers) Glucose EEG if seizure concern MRI brain only if high suspicion of CNS pathology
What is the cause of acute cerebellar ataxia in a child <3 years the resolves with conservative management?
Viral cerebellitis
What is the cause of ophthalmoplegia following diarrhoeal illness?
If immediate think botulism (typically symmetrical, dry mouth and associated with a descending weakness) If delayed think Miller-Fisher variant of GBS
What is the action of botulinum toxin?
Prevents synaptic release of Ach at the NMJ
What tumours cause anosmia?
Foster kennedy syndrome - olfactory groove meningiomas Esthesioneuroblastoma **Congential anosmia with hypogonadism = KALLMAN syndrome**
What is Mobius syndrome?
Congenital facial nerve paralysis. Also associated with complex opthalmoplegia, ptosis and lingual palsy.
What syndrome causes CN6+7 palsy with contralateral hemiparesis?
Gubler-Millard syndrome
What causes osteopetrosis?
A failure of osteoclasts to resorb bone resulting in diffuse hyperostosis causing blindness, deafness and cranial neuropathies.
What causes pulsatile exopthalmos?
CCF NF-1 with sphenoid wing dysplasia / orbital roof defect causing transmitted pulsations Vascular tumours
What causes pulsatile exopthalmos?
CCF NF-1 with sphenoid wing dysplasia / orbital roof defect causing transmitted pulsations Vascular tumours
What causes osteopetrosis?
A failure of osteoclasts to resorb bone resulting in diffuse hyperostosis causing blindness, deafness and cranial neuropathies.
What causes non-pulsatile exophthalmos?
Optic glioma
Optic nerve sheath schwannoma / neurofibroma
Optic nerve sheath meningioma
Lymphoma
Also think: Metastatic neuroblastoma or LCH in paeds.
Cavernous sinus thrombosis
Grave’s disease
What is Hand-Schuller-Christian syndrome?
LCH with DI, exophthalmos and lytic bone lesions.
What are the causes of ptosis?
CN3 palsy
Horner’s syndrome
Myaesthenia gravis (bilateral)
What are the main causes of macrocephaly?
Familial
Benign enlargement of the subarachnoid spaces / subdural spaces
Hydrocephalus
Which neurocutaneous syndromes cause megalencephaly?
NF
Congenital hypermelanosis
Hemi-megancephaly
(TS and Sturge-weber is less commonly)
Which condition has a cranial bruit in small children?
Vein of Galen malformation
What conditions cause pulsatile tinnitus?
CCF
DAVF
Pial AVM
Glomus jugulare
Hypertension
Hyperthyroidism
IIH / other causes of raised ICP
What causes numbness around the lips?
Low Ca
Syringobulbia
What does compression / damage to the spinal trigeminal tract cuase?
Loss of pain and temperature to the ipsilateral face with preservation of fine touch. The spinal trigeminal extends down to C2.
What does anterior cingulate retraction cause?
Akinetic mutism. Also seen with thalamic injury, mid corpus callosum injury and cerebellar vermis (?dentate nucleus) damage
What does anterior cingulate retraction cause?
Akinetic mutism. Also seen with thalamic injury, mid corpus callosum injury and cerebellar vermis (?dentate nucleus) damage
What does compression / damage to the spinal trigeminal tract cuase?
Loss of pain and temperature to the ipsilateral face with preservation of fine touch. The spinal trigeminal extends down to C2.
What causes numbness around the lips?
Low Ca
Syringobulbia
What are the main causes of macrocephaly?
Familial
Benign enlargement of the subarachnoid spaces / subdural spaces
Hydrocephalus
What are the causes of myelopathy?
Trauma Degenerative (disc disease / OPLL) Tumour - MSCC / paraneoplastic / leptomeningeal Vascular - haematoma / AVM / infarct Demyelinating - Transverse myelitis / MS / NMO (more than 3 levels) Metabolic - Vit B12 deficiency (associated with pernicious anaemia) Amyotrophic lateral sclerosis / primary lateral sclerosis
How do you test for Pernicious anaemia?
Schilling test - give radiolabelled Vit B12 without intrinsic factor and then with intrinsic factor and measure the amount of the radiolabelled Vit B12 in the urine
Where does the piriformis muscle attach?
From the VB of S2-3, through the greater sciatic notch to the greater trochanter
What is the root innervation to piriformis and what is its function?
L5/S1 and causes hip ext rotation
What is piriformis syndrome?
Where the piriformis muscle causes compression of the sciatic nerve
Test using the PACE test which is where resisted external rotation of the hip reproduces symptoms
How do you distinguish L4 radiculopathy from femoral nerve neuropathy?
Femoral neuropathy causes anterior thigh numbness, weak hip flexion (due to iliopsoas) and normal adductors.
L4 radiculopathy causes numbness of the medial leg (spares the thigh which is L3), has normal hip flexion power and weak adductors.
Note: both will have weak knee extension
What cells do motor fibres in the precentral gyrus arise from?
Pyramidal cells of Betz
What does an internal capsule lesion cause?
Pure motor hemiparesis without sensory impairment. Most commonly due to lacunar infarcts.
What is suggested by nocturnal back pain relieved by aspirin?
Osteoid osteoma / osteoblastoma
What is Patrick’s test for ankylosing spondylitis?
Compressing the pelvis in the lateral decubitus position causing pain suggests ankylosing spondylitis (sacroiliitis)
What is Reiter syndrome?
A reactive arthritis following a bacterial infection in patients that are HLA-B27 positive. Has non-joint involvment also e.g. skin lesions, uveitis etc.
What is a Schmorl’s node?
Herniation of disc through the endplate into the vertebral body
What is the nerve supply to tibialis anterior?
Deep peroneal nerve (L4/5)
How do you differentiate L5 radiculopathy and common peroneal nerve palsy as causes of foot drop?
Tibialis posterior (tibial nerve) and gluteus medius (superior gluteal nerve from the sacral plexus) are spared with common peroneal nerve injury but not L5 radiculopathy. This means that foot inversions and hip abduction are normal. Test hip abduction (gluteus medius function) with Trendelenburg sign when getting them to walk.
How do you differentiate deep, superficial and common peroneal nerve injuries?
Deep peroneal nerve injury causes a pure motor foot drop with loss of ankle eversion.
Superficial peroneal nerve injury causes a numb lateral leg but no foot drop. There is a weakness of eversion due to peroneus longus.
Common peroneal nerve injury causes both weakness and numbness.
What weakness pattern is seen with peripheral neuropathies?
Distal > proximal causing wrist and ankle drop
What muscle do you check for L2/3 root function?
Hip adductors. Supplied by the obturator nerve (L2,3,4).
How do you localise a sciatic nerve lesion?
Root lesion - paraspinal muscle weakness
Lumbar plexus - weakness of gluteus medius (hip abduction) and maximus (hip extension) but sparing of paraspinal muscles
Sciatic nerve (prox to common peroneal nerve branch) - biceps femoris (flexion of the knee) and gastrocnemius (plantar flexion) are weak
Tibial nerve (weakness of tibialis posterior so cannot invert the foot).
Deep peroneal nerve causes foot drop through weakness of tibialis anterior
Supfl peroneal nerve (weakness of ankle eversion but no foot drop)
What muscle do you check for L4 root function
Quadriceps femoris (L4) innervated by the femoral nerve
What is Bell’s cruciate paralysis?
Where a foramen magnum lesion causes upper limb but not lower limb weakness due to compression of the medulla at the site of the UL decussation but sparing the more laterally located LL fibres that decussate lower.
Which muscles do the superior and inferior gluteal nerves innervate?
Superior innervates the gluteus medius, minimus and tensor fasciae lata
The inferior gluteal nerve innervates gluteus maximus
What are the causes of hand atrophy/weakness?
Cervical myelopathy / radiulopathy
ALS
Central cord syndrome
Syrinx
Brachial plexus injury
Brachial plexus inflammation = parsonage turner syndrome
Peripheral nerve impingement (median / ulnar)
Thoracic outlet syndrome
What causes atrophy of the first dorsal interosseous?
C8/T1 radiculopathy
Lower brachial plexus involvement (pancoast / thoracic outlet syndrome)
Ulnar neuropathy (elbow or Guyon’s canal)
ALS / mutlifocal motor neuropathy
What is Adson test for thoracic outlet syndrome?
Turn head to ipsilateral side
Feel pulse
Raise ipsilateral arm
Feel if pulse dimishes.
*Reverse Adson test if you turn head to the other side
What is Eagle’s syndrome?
An enlarged styloid process causing glossopharyngeal neuralgia
What causes burning in the hands and feet?
Central cord syndrome
CRPS
Peripheral neuropathy (diabetes!)
Vascular causes (Raynaud’s / venous insufficiency)
What are the types of CRPS?
Type 1 = whole limb, no response to nerve block, trophic changes in the whole limb. Bone atrophy. Progressive.
Type 2 = single nerve invovlement. Has a precipitating event. Burning / allodynia.
What does Lhermitte’s sign signify?
Dorsal column pathology
(MS / SACD / Cervical myelopathy / Chiari)
What spinal level does the iliac crest demarcate?
L4/5 interspace (L4 spinous process)
Label the structures:
1 = S2 VB
2 = SI joint (synovial portion)
3 = SI joint (non-synovial portion)
4 = Sacral ala
5 = Iliac bone
6 = S2 root
7 = S3 root
8 = Multifidus
9 = Glut. maximus
10 = Glut. medius
Label the structures on the CT myelogram:
- Odontoid process
- C1 lateral mass
- Lateral neural arch
- Posterior neural arch
- CSF
- Spinal cord
- Anterior midline tubercle
- Foramen transversarium
- Dorsal rootlet
- Rectus capitus posterior major
- Semispinalis capitus
- Tubercle of the transverse ligament
What are the muscles of the suboccipital triangle?
Trapezius is more superficial. SCM being lateral. Both attach to the superior nuchal line
Then Semispinalis (medial) and splenius capitus (lateral)
Rectus capitus post. major - C2 spinous process to the inferior nuchal line
Inferior oblique - C2 spinous process to C1 lateral tubercle
Superior oblique - C1 lateral tubercle to inferior nuchal line
(The rectus capitus posterior minor attaches from the C1 lamina to the inferior nuchal line)
What are the muscle attachment at the back of the skull?
Label the structures:
- C4 VB
- Spinal cord
- C5 sup articular process
- C4 inferior articular process
- Lamina
- Spinous process
- Vertebral artery
- Facet joint
- C5 DRG
- Dorsal rootlet
- Ventral rootlet
- Longus coli
- Multifidus
- Semispinalis capitus
- Splenius captius
- IJV
17 ICA
What nerves supply the scalp and face?
- Supratrochlear (from V1)
- Supraorbital (from V1)
- Infratrochlear (from V1)
- External nasal (from V1)
- Infraorbital nerve (from V2)
- Lacrimal (from V1)
- Zygomaticotemporal (from V2)
- Zygomaticofacial (from V2)
- Auriculotemporal (from V3)
- Buccal (from V3)
- Mental (from V3)
- Greater auricular (C2/3)
- Transverse cervical (C4)
- Supraclavicular (C4)
- Greater occipital (C2)
- Lesser occipital (C2)
Where is the hypoglossal nerve during high ACDF approach?
Beneath the posterior digastric running between the ICA and IJV. Runs deep to mylohyoid on the surface of hyoglossus
How do you assess bony fusion in the spine?
In the absence of instrumentation lateral flexion-extension Xrays show lack of movement at that level
If there is instrumentation then CT is needed
What is the correlation between fusion and clinical outcome?
Not strong
What is osteoinduction?
The process of mesenchymal recruitment to develop osteoblasts and osteoclasts
What is osteogenesis?
The formation of new bone
What is osteoconduction?
A scaffold upon which new bone can form
Where is autograft taken from?
Bone taken during decompression
Iliac crest
Rib
Fibula
Risk of donor site morbidity (~30%)
Can be cancellous / cortical / both (tricortical) or marrow
Which windows are tcds performed through?
Temporal, orbital, suboccipital and submandibular
What are the different properties of cortical vs cancellous autograft?
Cortical provides mechanical stability
Cancellous is osteogenic, osteoinductive and osteoconductive
What is the most osteoinductive substance?
BMP
What are the risks of using fibula autograft?
Common peroneal nerve palsy
Ankle instability
How do you read a Vernier scale?
Align the 0 on the Vernier scale with the rule scan to get the mm distance. Then whichever of the Venier lines that lines up with the rule scale lines tells you the next decimal value.
In the picture, the answer is 2.1 mm as the 0 on the vernier is at 2 on the rule scale and the 1 on the vernier is in line with the rule scale.
Which sutures are braided and non-absorbable?
Silk and Ethibond
Which sutures are braided and absorbable?
Vicryl
Which monofilaments are non-absorbable?
Ethilon / Prolene
Which monofilaments are absorbable
Monocryl, PDS and cat gut
How does the Lindegaard ratio differentiate vasospasm from hyperaemia?
Spasm ratio severe >6 (3-6 is mild)
Hyperaemia ratio <3
Most reliable for MCA and basilar A vasospasm.
An MCA Vmean >180 cm/s suggests spasm or an increase in 20%
What range do fluorescein, 5ALA and ICG emit light?
520 nM Fluorescein
625 nM 5ALA
700-850 nM ICG
What is 5-ALA?
5 aminolevulinc acid
A precursor of protoporphyrin 9 in the heme synthesis pathway within mitochondria (so not seen in RBCs!)
Photobleaching occurs at an average of 1% per minute under UV light
What is Joule’s first law?
Heat = current density squared x resistance x time
What are cutting and coagulation diathermy setting?
Cutting = Pure continuous sine wave of low voltage that produces high temperature that vaporizes the tissue.
Coagulation = intermitted sine wave with a longer off-time i.e. low duty cycle and a higher voltage that produces a coagulation effect. Fulguration is when the coagulation voltage is high enough to create a zone of thermal damage.
What is a blend diathermy setting?
A waveform similar to coagulation with a higher duty cycle producing more cut and less coagulation.
What methods are used to identify the motor cortex?
Phase reversal (performed asleep) - a strip is placed traversing the central sulcus covering precentral and postcentral cortices. SSEPs are undertake with peripheral stimulation. Phase reversal of N20 to become P20 indicates the location of the central sulcus.
Direct cortical / subcortical stimulation (awake surgery)
How do you manage patients with pacemakers pre-operatively?
Pacemakers should be checked and reprogrammed to monitor mode prior to surgery so that they do not inadvertently discharge during surgery with diathermy use. Placing a magnet over the pacemaker can do this.
What is the difference between Floseal and Surgiflo?
Floseal has human thrombin and bovine gelatin
Surgiflo is porcine gelatin (spongistan is a solid version)
What is DuraGuard?
Bovine pericardium with glutaraldehyde
Why is partial aspiration of a cystic lesion undertaken?
To decompress the lesion, similar to debulking prior to dissection of the wall.
Complete aspiration is avoided to prevent being unable to find the lesion!
What causes severe brain swelling during surgery?
Extra-axial bleeding
ICH
Venous outflow obstruction
Vasodilation (check the pCO2!)
Diffuse cerebral oedema from stroke
How do you manage severe brain swelling?
Alert the anaesthetist: Elevate the head
Prevent neck vein kinking - place head in neutral position
Reduce the CO2 to between 30-35 mmHg
Drain CSF
Mannitol bolus (1g/Kg IV)
Deepen the sedation to induce burst suppression
Intraoperative US to identify an ICH that can be evacuated
Decompressive craniectomy
What is the risk of a post-op haematoma following craniotomy?
1%
What are the causes of a post-operative decline following craniotomy?
Cerebral oedema
Haematoma
Hydrocephalus (esp. if intraventricular/intracisternal)
Infarction
Pneumocephalus
Seizure
Why is intraoperative mapping performed?
To identify eloquent regions of brain such as motor and language cortices.
Mapping can be performed awake or asleep.
Which nerves are anaesthetised with a scalp block?
Supraorbital / supratrochlear
Auriculotemporal
Posterior auricular branch of the greater occipital
Greater and lesser occipital nerves
What stimulation settings do you use for cortical mapping?
Using a bipolar electrode:
50Hz
Biphasic square wave (2ms peak to peak)
Current 1-10 mA
A recording strip is also placed on the brain surface.
Start at a low current and stimulate for 3-5 seconds and observe for after discharges on the recording strip. Increase current until after discharges occur. Use this as the threshold for speech mapping looking for speech arrest, dysnomia, semantic and phonemic paraphasias
How do you place a patient in the park bench position?
Position the patient at the top of the table so the arm can extend down over the top.
Place a roll under the chest wall (not pushed into the axilla, as this may damage the brachial plexus).
Upper arm / shoulder are taped downward and forwards to open the working space.
Head placed in mayfield clamp looking 30 degrees to the floor.
Elevate the head 15 degrees.
Round bolster placed at the ASIS and flat bolster on the back.
Pillow in between the knees
Where does cortical stimulation result in speech arrest?
Pars opercularis / precentral gyrus
Where does cortical stimulation result in dysnomia?
Frontal and parietal operculum of the dominant hemisphere (and IFOF subcortically)
Where does cortical stimulation result in semantic paraphasias?
Inferior frontal, supramarginal and posterior temporal regions
Where does cortical stimulation result in phonemic paraphasias?
Superior temporal gyrus (and arcuate fasciculs)
What positioning options are there for posterior fossa approaches?
Prone / concorde
Park bench
Sitting
Advantages and disadvantages of the sitting position?
Advantage - CSF and blood drain from surgical site, gravitation retraction and enhanced venous drainage.
Disadvantage - Air embolism, fatigue, air embolism, pneumocephalus, sciatic nerve injury and reduced cerebral blood flow.
Why do venous emboli occur?
As the venous sinuses are non-collapsible and the negative pressure entrains air. This accumulates in the right atrium and creates an airlock preventing venous return to the heart.
Note a patent foramen ovale can cause a paradoxical air embolism resulting in a stroke!
How do you treat a venous air embolism?
Occlude the opening by placing a soaking wet swab over the field and flood the field with saline.
Lower the head initially
Jugular venous compression if accessible
Rotate the patient left side down (Durant’s manoeuvre)
Aspirate air from the right atrium via CVP
Ventilate with 100% O2
Use pressors and fluid to maintain BP
How do you perform a telovelar approach?
Suboccipital craniotomy and U-shaped dural opening.
The uvula is separated from the tonsils bilaterally.
The tonsils are retracted superiorly and laterally.
The PICA is visualised and protected.
The tela choroidae and inferior medullary velum are opened as the uvula is retracted.
The floor is protected by inserting a pattie.
What is the earliest sign of venous air embolism?
Reduction in end-tidal CO2
Describe the anatomical location of structures following a pterional approach with proximal splitting of the sylvian fissure.
Optic nerve
Carotid
Anterior choroidal
PCom
ACom complex
CN3
Carotid-oculomotor approach to basilar tip
How can you monitor for air embolism?
Precordial doppler
Where do you place the incision for a retrosigmoid craniectomy?
5 mm behind the digastric groove of the mastoid
What are the approaches to the third ventricle?
Transcortical (middle frontal gyrus for anterior 1/3 ventricle) - requires dilated ventricles
Transcallosal - anterior and posterior
Subfrontal - trans lamina terminalis through subfrontal or pterional approaches and transphenoidal for suprasellar lesions extending into third ventricle
Supracerebellar infratentorial
Suboccipital transtentorial
Describe the anatomy of the ventricles from an interhemispheric transcallosal approach
Orientation by identifying the thalamostriate vein and following it anteriorly to the foramen of Monroe.
How can the window through the foramen of Monroe be expanded?
Transchoroidal (medial to the choroid plexus through the tenia fornices)
Or
Interforniceal (between the left and right fornices)
What incision do you use to access a unilateral cerebellar hemisphere?
Mitre/hockey-stick incision. Starting from C2 up to the inion and across (below the transverse sinus) then curve down to the mastoid
Describe how you would perform an interhemispheric transcallosal approach for a colloid cyst
In an appropriately consented and anaesthetised patient.
I would apply the Mayfield clamp and position then supine with slight head elevation (10-15 deg). Registration of neuronavigation.
Linear bicoronal incision (or box flap) at the level of the coronal suture
6 cm AP (2/3 anterior to coronal suture and 1/3 behind) x 4 cm medial-lateral craniotomy straddling the midline to give control over the SSS. Position is planned to avoid sacrificing large cortical veins.
Dura flapped over the SSS
Interhemipheric dissection following the falx
Once the falx ends you see the cingulate gyri
Dissect between the cingulate gyri to visualised the pericallosal arteries
Dissection between the pericallosals through the corpus callosum from within 2cm of the genu ensuring not to enter a cavum septum pellucidum.
Where is the asterion?
Junction of the lambdoid, parieto-mastoid and occipito-mastoid sutures. It is an inconsistent marker for the transverse-sigmoid junction.
How do you perform a ventriculostomy following a pterional craniotomy?
Through Paine’s point: 2.5cm above and behind the sylvian fissure. Passed directly parallel to the floor of the anterior fossa.
This is used when there is significant brain swelling to allow CSF egress.
**RISK of hitting the caudate and damaging Broca’s area on the left. In which case modify the entry to be more anterior.
How do you seal mastoid air cells?
Pack them with bone dust mixed with bone wax
Where are Frazier and Dandy burr holes for ventriculostomy?
Frazier - 6 cm above and 3 cm lateral
Dandy - 3cm above and 3cm lateral (used in paediatrics)
How do you retract the cerebellum following retrosigmoid craniectomy?
Inferior retraction at the petrotentorial junction gives access to CN5
Medial retraction of the lateral cerebellar hemisphere gives access to CN7/8
Superior retraction gives access to the CN9/10/11
What forms the floor of the 4th ventricle?
The upper 2/3 are formed by the pons and lower 1/3 is formed by the medulla.
What are the approaches to the 4th ventricle?
Transvermian - through the inferior medullary velum to the fastigium. The superior medullary velum is not split. Risk of mutism, truncal ataxia and dysequilibrium.
Telovelar - through the cerebellomedullary fissure with elevation of the tonsil. Narrow corridor with limited rostal reach.
What are the main considerations following posterior fossa surgery?
Cranial nerve function (CN 7 & 10)
Respiratory rate and pattern
Hypertension must be avoided to prevent rebleed
Obstructive hydrocephalus
CSF leak
What is the name of the bicoronal incision?
Souttar incision
What are the approaches to lesions within the frontal horn or body of the lateral ventricle?
Interhemispheric transcallosal
Trans-middle frontal gyrus
What are the side effects of VIM stimulation?
Paraesthesia (too posterior - stimulation of lemniscal fibres entering the ventralis caudalis nucleus)
Dysequilibrium (due to ZI stim)
Dysarthria (too medial - stimulation of the medial Vim) or too lateral if also associated with muscle contractions - stimulation of the internal capsule)
Ataxia (too ventral and medial - stimulation fo the brachium conjunctivum)
High voltages needed for tremor suppression (too anterior due to stimulation of the ventralis oralis posterior)
Phosphenes (too deep - optic tract stimulation)
What side effects are expected with the following electrode locations for Vim stimulation?
a - electrode is too anterior and within the VOP - requires high voltages to induce tremor suppression
b - electrode is too short within the Vim - will likely not to result in any tremor suppression.
c - electrode too posteroir and within the ventralis caudalis nucleus - will likely results in paraesthesias due to leminiscal fibre stimulation
What side effects are expected with the following electrode locations for Vim stimulation?
a - medial location within the Vim. Likely to result in dyarthria.
b - deep location stimulating the ZI and brachium conjunctivum. Likely to cause ataxia.
c - lateral location so within the internal capsule. Likely to cause dysarthria and facial pulling movements/dystonia.
What are the approaches to lesions within the temporal horn of the lateral ventricle?
Trans-middle temporal gyrus
Trans-temporal horn following temporal pole resection
Label the adjacent structures to the STN (axial and coronal images shown)
Superior = ventralis oralis anterior / ZI (stim results in tremor suppression)
Inferior = Substantia nigra (stim results in akinesia)
Medial and deep = midbrain / CN3 nuclus (double vision and gaze deviation)
Anterior or Lateral = internal capsule (dysarthria and muscle contraction)
Posterior = (perspiration and mydriasis)
What are the side effects of incorrectly placed DBS electrodes?
Based on the target:
STN / VIM / GPi
How do you resect a choroid plexus papilloma?
The ventricles are enlarged due to overproduction of CSF.
The lateral ventricle is approached through a transcortical route. The vascular pedicle arising from the choroidal arteries is coagulated and cut (Vineyard technique)
During colloid cyst resection how do you prevent traction on the fornix?
The colloid cyst should be aspirated / debulked.
The cysts wall should be delivered into the lateral ventricle through the foramen of monroe.
The stalk attachment to the roof of the third ventricle should be coagulated and cut.
What is ‘Syndrome of the trephined’?
Headache and neurological deficit (incl motor, speech and executive function) associated with the brain below usually 6 months after craniectomy due to atmospheric pressure on the brain. This is thought to cause venous compression and altered CSF dynamics.
During transoral odontoidectomy, do you decompress or fuse from the back first?
Decompress first and do OC fixation later as the positioning for OC fixation can cause neurological compression.
What specific risk with MEPs should be consented for?
Seizures!
What screws are used with occipital plates?
Cortical screws (narrow pitch) with blunt flat tips to prevent dural penetration
What procedures are performed stereotactically?
Biopsy
Catheter placement
Electrode placement
Lesioning
Cyst/haematoma aspiration
SRS
What is the yield from stereotactic brain biopsy?
80-95% (lower rates with AIDS)
What are the indications for DBS?
Movement disorders (PD, ET and dystonia)
Epilepsy (ANT, Centromedian, Hippocampus)
Pain (Thalamus)
Psychiatric (OCD, Tourette’s, depression)
Which PD patients are eligible for DBS?
- Retractory to medical therapy
- Levodopa-induced dyskinesia
- Gait and postural instability (PPN)
What are the contraindications to DBS for PD?
Dementia
Risk of ICH (coagulopathy / uncontrolled hypertension)
Ipsilateral hemianopsia (due risk of complete blindness)
Age >85 years
Secondary Parkinson’s (MSA / PSP / olivopontocerebellar atrophy)
Which symptoms improve most following DBS for PD?
Dyskinesia (due to drug reduction) 90%
Bradykinesia 85%
Rigidity 75%
Tremor 60%
What electrodes are used for DBS?
Platinum iridium contacts 1.5 mm length spaced by 1.5 mm. Diameter 1.2 mm.
Stimulation parameters: pulse width 75 μs, frequency 150 Hz.
With a well-placed electrode, tremor arrest can be achieved at 0.5 to 2.0 volts. Suppression thresholds of 4 volts or greater suggest that repositioning of the electrode may be necessary.
What follow up do patients with VHL need?
1) Opthalmology
2) Measurement of urine or plasma fractionated metanephrines (to screen for pheochromocytoma).
3) Audiology
4) Abdominal ultrasound for renal tumors
5) MRI of the brain and spinal cord
