11- Paediatric Neurology (2/3) Flashcards
intracranial pressure
‘The pressure within the cranium of the skull’
monroe kellie doctrine
** sum of volumes of (1) Brain, (2 CSF and (3) Intracranial blood is constant**
- Skull is a rigid box
- If one of these components is lost e.g. a bleed or tumour (SOL) , other components of this volume will need to reduce to make sure the sum of volume stays constant
intracranial elastance curve
- As intracranial volume increases initially ICP stays the same due to compensatory mechanisms
- After mechanisms exhausted the ICP will increase
ICP and (1) Blood
Need constant blood supply to supply neurones and brain tissue. Incredibly sensitive to low oxygen.
Cerebral perfusion pressure (CCP) represents cerebral blood flow.
- CPP = Mean arterial pressure (MAP)- ICP
If ICP increased, perfusion of the brain decreases (without cerebral autoregulation)- BV will vasodilate
cerebral autoregulation
- If MAP increases then CPP increases, triggering cerebral autoregulation to maintain cerebral blood flow (vasoconstriction)
- If ICP increases then CPP decreases, triggering cerebral autoregulation to maintain cerebral blood flow (vasodilatation) will result in having to increase MAP- therefore hypertension
- If CPP <50 mmHg then cerebral blood flow cannot be maintained as cerebral arterioles are maximally dilated
- ICP can be maintained at a constant level as an intracranial mass expands, up to a certain point beyond which ICP will rise at a very rapid (exponential) rate
- Damage to the brain can impair or even abolish cerebral autoregulation
ICP and (2) CSF
- CSF produced by the choroid plexus into the lateral ventricles
- Around 500mls produced each day
- Homeostasis, protection, buoyancy and waste clearance
ICP and (3) brain
- If herniating, usually high pressure inside
- Types of herniation
o Subfalcine herniation (commonest)
o Tonsillar herniation (aka coning)
o Uncal herniation
raised ICP is due to
- Too much blood
- Too much CSF
- Too much brain
presentation of RICP
- Headaches (At night time, waking and bending over)
- Nausea + vomiting
- Visual disturbances e.g. double vision
- Drop of >2 in GCS
o Confusion
o Seizures
o Amnesia - Papilledema
- Focal neurological signs
o E.g. CN3 palsy – papillary dilatation - Abnormal posturing (decorticate, decerebrate)
- CushinGs reflex
3 Primary signs of RICP
Cushings triad
- hypertension
- bradycardia
- irregular breathing
LATE SIGNS
pathophysiology of (1) too much blood
1) Too much blood within cerebral vessels (rare)
- Raised arterial pressure- malignant hypertension
- Raised venous pressure- SVC obstruction
2) Too much blood outside the cerebral vessels (haemorrhage)
- Extradural
- Subdural
- Subarachnoid
causes of too much blood within cerebral vessels
- malignant hypertension
- superior vena cava obstruction
Malignant (accelerated) hypertension
- Systolic >180mmHg or Diastolic >120mmHg
* Usually renal cause in children - Signs of target organ damage
o Retinal haemorrhages
o Encephalopathy
o Left ventricular hypertrophy
o Reduced renal function - Urgent referral
Superior vena cava (SVC) obstruction
- Reduction in venous return from head & neck & upper limbs
- Most common cause is malignancy
o Non-Hodgkin’s in children - Oncology Emergency
- Presentation
o Local oedema of the face and upper limbs
o Dilated veins in the arm and neck and anterior chest wall
o SoB
o Difficulty swallowing
o After lifting arms the signs will get worse
(2) Too much CSF also known as
hydrocephalus
hydrocephalus background
- CSF build up abnormally in the brain and spinal cord
- Due to over-production or problems draining or absorbing CSF
hydrocephalus pathophysiology
*- Congenital
- Acquired
- Non-communicating vs communicating
**
hydrocephalus pathophysiology
*- Congenital
- Acquired
- Non-communicating vs communicating
**
congenital hydrocephalus
- Present at birth
- Genetic and non-genetic factors e.g. mutation in L1CAM gene linked to aqueductal stenosis
pathophysiology of congenital hydrocephalus
- Most common cause is aqueductal stenosis ->Insuff drainage of CSF
- Cerebral aqueduct which connect third and fourth ventricle is stenosed
presentation of congenital hydrocephaly
- Enlargement of head circumference- sutures not fused – occipito-frontal circumference (macrocephaly)
Bulging from anterior fontanelles
Poor feeding and vomiting
Poor tone
Sleepiness - Downward gaze
- Delay in neurological development
management of hydrocephalus
- VP shunt- ventricles- peritoneum
- VA shunt- ventricles- atria
Normal CSF Physiology
There are four ventricles in the brain: two lateral ventricles, the third and the fourth ventricles.
The ventricles contain CSF.
The CSF provides a cushion for the brain tissue. CSF is created in the four choroid plexuses (one in each ventricle) and by the walls of the ventricles.
CSF is absorbed into the venous system by the arachnoid granulations.
acquired causes of hydrocephaly
Acquired causes
- Intraventricular haematoma
- Tumour
- Infection
- Trauma
too much CSF caused by obstruction (non-communicating)
too much CSF- communicating hydrocephalus
Too much CSF- Communicating hydrocephalus
* Overproduction of CSF or
* Reduced absorption of CSF
Examples of cause
- Choroid plexus papilloma
- Infection and inflammation leading to scarring at subarachnoid space
Ventriculoperitoneal Shunt
Placing a VP shunt that drains CSF from the ventricles into another body cavity is the mainstay of treatment for hydrocephalus. Usually the peritoneal cavity is used to drain CSF, as there is plenty of space and it is easily reabsorbed. The surgeon places a small tube (catheter) through a small hole in the skull at the back of the head and into one of the ventricles. A valve on the end of this tube is placed subcutaneously, and a catheter on the other side of the valve runs under the skin into the peritoneal cavity. The valve helps to regulate the amount of CSF that drains from the ventricles.
VP Shunt Complications
* Infection
* Blockage
* Excessive drainage
* Intraventricular haemorrhage during shunt related surgery
* Outgrowing them (they typically need replacing around every 2 years as the child grows)
(3) too much brain
- Usually causes by cerebral oedema= swelling of the brain
- 4 types
example causes of too much brain
- brain tumour e.g. primary, metastatic and intra
- cerebral abscess
- hypoxic brain injury causing oedema
investigations for raised ICP
Bedside
- vital signs
- ECG
- fundoscopy
Bloods
- FBC
- UEs
- CRP
- clotting
- Group and save
- cross match
- blood culture
Imaging
- CT scan
- MRI
CT head scan indication
- Acute presentation
e.g. Head injury - Chronic presentation
management of RICP
visual field defects
- Named based on the area of visual loss rather than site of lesion
e.g.
monocular blindness
bitemporal hemianopia
homonomous hemianopia
causes of visual field defects
epilepsy
cerebral palsy
tumour
stroke
anatomy of the central visual pathway
comprised of:
1. The optic nerve (CN II)
2. The optic chiams
3. The optic tracts
4. Optic radiations
the optic nerve (CN II)
- Split into diff divisions (different fibres of the retina)
- Temporal (lateral)- orange
- Nasal (medial)- green
- Also have up and down
otpic chiasm
- Nasal fibres decussate
- Temporal fibres remain ipsilateral
optic tracts
- From optic chiasm to lateral geniculate nucleus (LGN
- Contains temporal fibres from the ipislateral side
- Contains nasal fibres from tbe contralateral side
optic radiations
From LGN to primary visual cortex (x2 ) in the occipital lobe (x2 lobes)
- 2 routes to the occipital lobe
1. Superior route via the parietal (superior optic radiations)
- Continuation of superior quadrant fibres (temporal and nasal)
- ‘Baums loop’
2. Inferior route via the temporal (inferior optic radiations)
- Continuation of inferior quadrant fibres (temporal and nasal)
- “meyes loop’
visual fields
Visual fields relate to peripheral vision (also called temporal and nasal). Each eye has its own set of visual filed
- These overlap to form binocular vision
- Good for depth perception
LIGHT TRAVELS IN STRAIGHT LINES… therefore:
- If we want to detect something in the temporal visual field, light will travel through the pupil straight to the nasal retinal fibres (temporal visual field detected by nasal retinal fibres)
- If we want to detect something in the nasal visual field, light will travel through the pupil straight to the temporal retinal fibres (nasal visual field detected by temporal retinal fibres)
monocular blindness
Background
- blindness in one eye
Causes
- Optic nerve lesion
Pathophysiology
- lesion disrupts tmeproal and nasal fibres on the ipsilateal (same) side affected and vision lost
bitemporal heminanopia
Background
- loss of temporal vision
- ‘tunnel vision’ only
Cause
- pituitary adenoma
Pathophysiology
- nasal fibres on both sides affected
- temporal visual field loss on both sides
Homonymous hemianopia
background
- loss of both left or loss of both right
Cause
- lesion of the optic tract on the right or left hand side
Pathophysiology
- Left nasal retinal fibres (contralateral) and right temporal retinal fibres (ipsilateral) affected
- Left temporal (contralateral) visual field lost and right nasal (ipsilateral) field loss
- ‘left homonomous hemianopia’- even though lesion is on the right- due to decussation
o Name the visual defect on visual loss not lesion
Optic radiation lesion
- Superior visual fields are detected by inferior retinal fibres
- Inferior visual fields are detected by superior retinal fibres
examples:
- Homonymous inferior quadrantanopias
- Homonymous superior quadrantanopias
Homonomous inferior quadrantanopia (left)
Lesion on right superior optic radiation (parietal lobe)
- Superior ipsilateral temporal fibre affected
o Loss of inferior nasal visual field
- Superior contralateral nasal fibre affected
o Loss of inferior temporal visual fields
Homonomous superior quadrantanopia (left)
- Inferior temporal fibres on ipsilateral side affected
o Loss of superior nasal visual field - Inferior nasal fibre on contralateral side is affected
o Loss of superior temporal visual field
