Neurosurgery Flashcards
Ventricular system
Paired lateral ventricles
Communicate by foramin of Munro with third ventricle
Third ventircle communicates via the aqueduct to the foruth ventricle
Outflow foramina: Luschka, and Magendie connect with basal and subarachnoid spaces
Large CSF cisterns around the base of the brain (e.g. cisterna magna, cerebellopontine cistern).
Anterior cerebrlal artery supplies
Frontal lobe and medial parts of parietal lobes
Middle cerebral artery supplies
Posterior frontal region and most of temporal and parietal regions
Posterior circulation supplies
Brain stem
Cerebellum
Occipital lobes
Inferior part of temporal lobes
End-arteries –> well defined stroke syndromes
Paired vertebral arteries –> basilar artery –> paired posterior cerebral arteries
Posterior cerebral arteries communicate with the anterior circulation through the posterior communicating arteries
In a normal supine adult, ICP is the same as the CSF pressure
Opening pressure of LP = ICP
Cerebral perfusion pressure (CPP)
= MAP - ICP
Why do you get a brady with raised ICP?
Rising ICP
Cerebral perfusion pressure = MAP - ICP
To achieve CPP, MAP increases as ICP increases
Increased MAP –> reflex bradycardia
Cerebral perfusion pressure (CPP)
= MAP - ICP
CPP of > 60 mmHg is generally required to sustain adequate cerebral perfusion
Sub-falcine herniation (cingulate gyral)
Caused by para-sagittal mass
Ipsilateral cingulate gyrus may herniate beneath the free edge of the falx
Anterior cerebral artery may be compressed leading to hemispheric infarction
Otherwise, reduced GCS is only clinical sign
Tentorial herniation
Large ipsilateral lesion
Medial part of temporal lobe is pushed down through tentorial notch –> becomes wedged between tentorial edge and midbrain
Cerebral peduncle is pushed against sharp tenrotial edge
Midbrain and uncus become wedges at tentorium
Aqueduct is compressed , obstructing CSF flow
Obstruced venous flow –> midbrain haemorrhage
Uncul herniation:
- Falling GCS
- Motor component of GCS becomes asymmetrical
- Ipsilateral 3rd nerve palsy, dilated an ddixed pupil
- Hypertension and bradycardia
- Respiratory arrest
Tentorial (uncal) herniation
Large ipsilateral lesion
Medial part of temporal lobe is pushed down through tentorial notch –> becomes wedged between tentorial edge and midbrain
Cerebral peduncle is pushed against sharp tenrotial edge
Midbrain and uncus become wedges at tentorium
Aqueduct is compressed , obstructing CSF flow
Obstruced venous flow –> midbrain haemorrhage
Uncul herniation:
- Falling GCS
- Motor component of GCS becomes asymmetrical
- Ipsilateral 3rd nerve palsy, dilated an ddixed pupil
- Hypertension and bradycardia
- Respiratory arrest
Foraminal (tonsillar) herniation
Lesion in posterior fossa
Causes cerebellar tonsills and midbrain to be pushed down through foramen magnum
Cerebellar impaction –> medulla compression
Clinical features:
- Rapid reduction in GCS
- Acute hypertension
- Bilateral extensor responses
- Bilateral fixed and dilated pupils
- Respiratory arrest
(Can be caused by LP in raised ICP –> coning)
Berri aneurysms
85% in anterior circulation
Nimodipine
Medical management of SAH
Alonside maintaining CCP and haemodilution
Avoid hypotension and fever - associated with poorer outcome.
Amyloid angiopathy
Common cause of intracerebral bleed
Coma
Defined as GCS of 8 or less
Indications for haematoma evacuation
> 5mm midline shift
Significant impairment of GCS
Protracted headache or vomiting
Intracranial haematoma risk pattern
No skull fracrure, GCS 15 –> 1 in 6,000
Skull fracture, GCS 15 –> 1 in 30
GCS 14 or less –> 1 in 4
Cervical spinal trauma
Commonly subluxation C5 on C6
Glioblastoma
Grade IV
Gliosarcomas
Grade IV
Anaplastic astrocytoma
Grade III
Anaplastic oligodendroglioma
Grade III
Astrocytoma
Grade II
Oligodendroglioma
Grade II
Ependymoma
Grade II
Pilocystic astrocytoma
Grade I
Dysembroplastic neuroepithelial tumour
Grade I
Ganglioma
Grade I
Shwannomas
Cranial nerve tumour
Nearly all affect the vestibulocochlear nerve
Grows and expands within internal auditory meatus
Cranial nerve VII and VIII become compressed as it grows into cerebellopontine angle
Early VIII th nerve symptoms:
- Progress deafness
- Tinnitus
- Vertigo
Larger tumours may involve the trigeminal nerve, eading to diminished facial sensation, as well as the pons and cerebellum, leading to ataxia and nystagmus.
Compression of fourth ventricle –> hydrocephalus
Prostate cancer metastasis
Commonly mets to cranium itself
NOT brain parenchyma
Galidium contrast doesn’t cross BBB so…
In areas of pathology there is breakdown of the BBB
–> uptake by tumours
Meningiomas are mesodermal in origin hence don’t have BBB —> they will take up contrast depist being only Grade I
Brain Primary
Primary cerebral tumours arise from:
supporting cells of the brain (gliomas)
from the walls of ventricles (ependymomas)
from the roof of the fourth ventricle (medulloblastomas).
Brain Primary
Primary cerebral tumours arise:
Supporting cells of the brain (gliomas)
Walls of ventricles (ependymomas)
Roof of the fourth ventricle (medulloblastomas).
Paediatric primary brain tumours
Age <2: Teratomas, Astrocytomas, PTENs
Occur anywhere
Age 2 - 15:
Usually PTENs (primitive neuroectodermal tumours) (also known as medulloblastomas when in posterior fossa), astrocytomas and ependymomas
Most common site is posterior fossa
Management of paediatric brain tumours
Surgery alone is not curative in High Grade tumours
Combination of surgery, chemotherapy and radiotherapy used
Radiotherapy not suitable for children under 3 –> damages developing brain
Age 3- 8: Radiotherapy may cause loss of IQ and other neurodevelopmental delays
Open spinal dysraphism
Spina bifida aperta
Myelomenigocoele
Open spinal defect with LMN signs, weakness and numbness below lesion and a neuropathic badder
Often develop hydrocephalus post closure and require a ventriculoperitoneal shunt
90% have malformation of hindbrain: Chiari II –> respiratory and feeding difficulties
Also develop scoliosis
Closed spinal dysraphism
Spina bifida occulta
Encompasses lesions: Lipomyelomeningoceole, meningoceole, tight filum terminale syndrome, sinus tract and intradural dermoids, split cord malformations and cuadal agenesis
Often asymptomatic
Later neurological deterioration or bladder dysfunction are due to tethering of the developing cord at the lesion site
Mx: surgical untethering
Individuals do not develop hydrocephalus and
there is no association with the Chiari malformation
Causes of hydrocephalus
Osbtruction - non-communication
- Congenital: aqueduct stenosis
- Tumour
- Arachnoid adhesions or fibrosis secondary to intraventricular haemorrhage or SAH
Communicationg / external
- Ventricular system is patent
- There is reduced flow through basal cisterns or absrobtion of CSF by arachnoid granulations
- -> commonly due to fibrosis post meningitis, SAH, or sagittal sinus thrombosis
Over-production
-Choroid plexus papilloma
Gait ataxia, Incontinence and Cognitive decline
Normal pressure hydrocephalus
Craniosynostosis
Premature closure of / absence of cranial suture
Premature fusion of sagittal suture: Scaphocephaly
Premature fusion of coronal suture: Plagiocephaly
Dermal sinuses
Squamous epithelium communicate with intracranial cavity
Mostly occipital region
Associated with inclusion dermoids
Complications of chronic disc herniation
Nerve root compression: lateral recess stenosis
Cord compression: Spondylitic myelopathy
Cauda equina: Lumbar canal stenosis
Pain along root of compression and diminished sensation in roots below
Mx of disc prolapse
If mild causing radiculopathy: conservative +/- delayed micropdiscectomy at 6 weeks
If posterior rupture into canal: urgent removal and plating
