My Clinical Notes

 

• Primary haemorrhages within the epidural or subdural space are associated with trauma
• Haemorrhages within the parenchyma or subarachnoid space are often manifestations of cerebrovascular disease, although trauma can also cause haemorrhage at these sites

 

Intracerebral (intraparenchymal) haemorrhage

 

• Non traumatic intracerebral haemorrhage occurs most commonly in middle to old age
• Peak incidence around 60 years
• Mostly caused by rupture of a small intraparenchymal vessel
• Hypertension is the most common underlying cause
• Abnormalities in vessel walls caused by hypertension;
  • Accelerate atherosclerosis in larger vessels
  • Hyaline arteriolosclerosis in smaller vessels
  • Proliferative change and necrosis in arterioles
• Results in weakness and increased susceptibility to rupture
• Chronic hypertension can be associated with minute aneurysms termed Charcot-Bouchard microaneurisms which may rupture
• Occur in vessels smaller than 300um in diameter most commonly within the basal ganglia
• These differ from the saccular aneurisms associated with larger vessels
• Other factors which may contribute to non traumatic haemorrhage
  • Systemic coagulation disorders
  • Open heart surgery
  • Neoplasms
  • Amyloid angiopathy
  • Vasculitis
  • Fusiform aneurisms
  • Vascular malformations

 

Morphology

• Hypertensive intraparenchymal haemorrhage may originate in the;
  • Putamen
  • Thalamus
  • Pons
  • Cerebellum
  • Cerebrum
• When haemorrhages occur in the basal ganglia or thalamus there are called ganglionic haemorrhages
• When they occur in the cerebral hemispheres they are called lobar haemorrhages
• Acute haemorrhages are characterised by bleeding with compression of the surrounding parenchyma
• Old haemorrhages show a cavity of destruction with a brownish coloured rim which consists microscopically of a core of clotted blood surrounded by tissue showing anoxic neuronal and glial cell changes and well as oedema. Eventually the oedema resolves and macrophages infiltrate and the reactive astrocytes proliferate around the rim of the lesion
• Lobar haemorrhages may occur in the setting of;
  • Haemorrhagic disposition
  • Neoplasms
  • Drug abuse
  • Infection
  • Vasculitis
  • Cerebral amyloid angiopathy (amyloid protein deposits around cerebral vessels)

 

Subarachnoid haemorrhage and rupture of saccular (berry) haemorrhage

 

• Rupture of berry aneurisms is the most common cause of SAH
  • SAH may also result from;
  • Traumatic hematoma
  • Rupture of hypertensive intracerebral haemorrhage into the ventricular system
  • Vascular malformation
  • Haematological disturbances
  • Tumours

 

• Berry aneurisms are the most common type of intracranial aneurism
• Other types include;
  • Atherosclerotic (fusiform, mostly of the basilar artery)
  • Mycotic
  • Traumatic
  • Dissecting
• All apart from atherosclerotic are most common in the anterior circulation

 

Pathogenesis of berry aneurisms

• Aetiology unknown
• Majority occur sporadically
• Increased risk among certain heritable disorders;
  • Autosomal dominant polycystic kidney disease
  • Vascular type Ehlers-Marfan syndrome
  • Neurofibromatosis type I
  • Marfan’s syndrome
• Associated with smoking and hypertension

 

 

Morphology

• Thinned walled outpouching at an arterial branch point along the Circle of Willis  or a major vessel just beyond
• Measure a few mm to 2-3cm
• Bright red shiny surface and thin translucent wall
• Rupture usually occurs at the apex of the aneurism with bleeding into the subarchnoid space or brain or both

 

• Rupture is associated with acute increases in intracerebral pressure
• Sudden, excruciating headache and rapid LOC
• In the acute period vasospasm occurs which can lead to ischaemic injury
• In the healing phase meningeal fibrosis and scarring can occur which may obstruct CSF flow or reabsorption

 

Epidural haemorrhage

 

• Epidural space is a potential space as the dura is fused with the periosteum
• Vessels that course within the dura, most notably the middle meningeal artery are vulnerable to injury particularly skull fractures
• Once a vessel has been torn, the accumulation of blood under arterial pressure can cause separation of the dura from the skull
• The expanding haematoma has a smooth inner contour which compresses the brain surface
• Patients can be lucid for several hours before the development of neurological signs

 

Subdural haemorrhage

 

• The space beneath the dura mater and the arachnoid  layer is also a potential space
• Bridging veins travel from the surface of the cerebral hemispheres through the subarachnoid space and subdural space to empty with dural vessels into the superior sagittal sinus
• These vessels are prone to tearing along their course through the subdural space and are the source of bleeding in most subdural haematomas
• Displacement of the brain following trauma tears the veins at the point they penetrate the dura
• In elderly patients with brain atrophy, the bridging veins are stretched and the brain has additional space for movement, hence why these patients are at particular risk

 

 

 

 

 

 

CNS trauma

 

• The magnitude and distribution of a traumatic brain injury depends upon;
  • The shape of the object causing the trauma
  • The force of impact
  • Whether the head is in motion at the time

 

• The physical forces associated with head injury may result in;
  • Skull fractures
  • Parenchymal injury
    • Concussion
    • Contusion
    • Laceration
  • Vascular injury

 

Skull fractures

 

• Fractures that cross suture lines are termed diastatic
• A displaced skull fracture is when a fragment of bone is displaced into the cranial cavity by a distance greater than the thickness of the bone
• Basal skull fractures typically result from blows to the occiput or sides of the head rather than the vertex
• Signs of a basal fracture include;
  • Orbital or mastoid haematomas
  • CSF discharge from the nose of ear
• Falls following LOC general result in frontal skull fractures
• Trauma which occurs when the individual is awake often results in a blow to the occipital portion of the skull

 

Parenchymal injuries

 

Concussion

• Clinical syndrome of altered consciousness secondary to head injury
• Typically brought about by change in momentum of the head
• Instantaneous onset of neurological dysfunction including;
  • LOC
  • Temporary respiratory arrest
  • Loss of reflexes
• Neurological recovery is complete but amnesia for the event can persist and neuropsychiatric problems can occur
• Pathogenesis is unclear but may be due to;
  • Depolarisation due to excitatory amino acid mediated ionic fluxes across cell membranes
  • Depletion of mitochondrial ATP
  • Alterations in vascular permeability

Direct parenchymal injury;

Lacerations – tearing of tissue

Contusions – bruising

 

• A blow to the surface of the brain transmitted through the skull, leads to;
  • Rapid tissue displacement
  • Disruption of vascular channels
  • Subsequent haemorrhage
  • Tissue injury
  • Oedema
• The crests of gyri are most susceptible whereas the cerebral cortex along the sulci are less vulnerable
• Most common areas of damage;
  • Frontal lobes along the orbital gyri
  • Temporal lobes
• Contusions are less frequent over occipital lobes, brainstem or cerebellum unless associated with fracture – fracture contusions

 

• Damage can be at the point of contact – a coup injury, or diametrically opposite it – a contrecoup injury. Both of these are described as contusions

 

Morphology

• Contusions
  • Wedge shaped on cross section, with the broad base spanning the surface
  • Histological appearance;
    • Oedema and haemorrhage early
    • Neuronal cells show signs of injury from about 25hr
    • Axonal swelling can develop
    • Inflammation occurs with neutrophils followed by macrophages

 

Diffuse axonal injury

• White matter damage
• Particularly affects;
  • Corpus callosum
  • Paraventricular areas
  • Hippocampal areas
  • Brainstem
• Axonal swelling is indicative of diffuse axonal injury as is focal haemorrhagic lesions
• Angular acceleration alone can be sufficient without impact
• Due to mechanical forces damaging the integrity of the axon at the node of Ranvier with subsequent alterations in axoplasmic flow
• Axonal swelling occurs within hours of injury
• Later there are increased numbers of microglia and subsequent degeneration of the involved fibre tracts

 

This entry was posted on Sunday, November 4th, 2007 at 5:30 pm and is filed under Neurology. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.