Primary intracerebral haemorrhage

Primary intracerebral haemorrhage (PICH) is somewhat more frequent than subarachnoid haemorrhage, the incidence increases with age, and it is probably more common in the Japanese and Chinese than in Whites (Section 27.2.4). It is most commonly due to intracranial small vessel disease associated with hypertension, cerebral amyloid angiopathy, and intracranial vascular malformations, but there is usually a combination of different factors operating in any one individual, e.g. hypertension and cerebral amyloid angiopathy, therapeutic thrombolysis and a vascular malformation, etc. (Warlow et al. 2000b).

Less common causes include saccular aneurysms; haemostatic defects, particularly induced by anticoagulation (Hart et al. 1995), therapeutic thrombolysis, perhaps with cerebral amyloid angiopathy (Simoons et al. 1993; Fibrinolytic Therapy Trialists' Collaborative Group 1994), and possibly antiplatelet drugs (He et al. 1998); cerebral vasculitis; and drug abuse (Kase 1986; Caplan 1988).

The site of PICH, shown on CT, provides some clue to the cause; ‘hypertensive’ haemorrhages tend to occur slightly more in the basal ganglia, thalamus, and pons, while lobar haemorrhages (i.e. superficial in cerebrum) tend to be somewhat more often due to cerebral amyloid angiopathy, vascular malformations, and haemostatic failure (Schutz et al. 1990; Molinari 1993). Occasionally PICHs occur in different parts of the brain simultaneously, or over a short period of time (Table 27.17). Rarely, PICH is familial:

Causes of simultaneous and multiple spontaneous intracerebral haemorrhages

  • Cerebral amyloid angiopathy
  • Metastases
  • Haemostatic defect
  • Thrombolytic drugs
  • Intracranial venous thrombosis
  • Inflammatory vascular disease
  • Intracranial vascular malformations
  • Malignant hypertension
  • Eclampsia
  • Multiple haemorrhagic infarcts (usually embolic from the heart)
  • Occult head injury
  • Drug abuse

It has previously been assumed that bleeding occurs abruptly and is limited, more or less at once, by the increasing pressure in the surrounding brain tissue. Quite commonly, however, continuing or early rebleeding visible on CT does occur within hours of stroke onset, and can cause deterioration (Brott et al. 1997).

Perhaps the initial haemorrhage sets off an ‘avalanche’ of surrounding secondary haemorrhages by distorting the microvasculature. In addition, early deterioration can be due to ischaemia and oedema around the haematoma (Mendelow 1991). Some brainstem haemorrhages evolve surprisingly subacutely, particularly those caused by a vascular malformation (O'Laoire et al. 1982; Howard 1986).

Any large haematoma may cause brain shift, transtentorial herniation, brainstem compression, and raised intracranial pressure. Haematomas in the posterior fossa are particularly likely to cause obstructive hydrocephalus. Rupture into the ventricles, or on to the surface of the brain is common (so causing blood to appear in the subarachnoid space and lumbar CSF).