Otogenic brain abscesses

Otogenic brain abscess:

Otogenic brain abscess always develop in the temporal lobe or the cerebellum of the same side of the infected ear. Temporal lobe abscess is twice as common as cerebellar abscess. In children nearly 25% of brain abscesses are otogenic in nature, whereas in adults who are more prone to chronic ear infections the percentage rises to 50%. The routes of spread of infection has already been discussed above, the commonest being the direct extension through the eroded tegment plate. Although dura is highly resistant to infection, local pachymeningitis may be followed by thrombophlebitis penetrating the cerebral cortex, sometimes the infection could extent via the Virchow - Robin spaces in to the cerebral white matter. Cerebellar abscess is usually preceded by thrombosis of lateral sinus. Abscess in the cerebellum may involve the lateral lobe of the cerebellum, and it may be adherent to the lateral sinus or to a patch of dura underneath the Trautmann's triangle.

Diagram showing evolution of brain abscess

Stages of formation of brain abscess:

Stage of cerebral oedema: This is infact the first stage of brain abscess formation. It starts with an area of cerebral oedema and encephalitis. This oedema increases in size with spreading encephalitis.

Walling off of infection by formation of capsule: Brain attempts to wall off the infected area with the formation of fibrous capsule. This formation of fibrous tissue is dependent on microglial and blood vessel mesodermal response to the inflammatory process. This stage is highly variable. Normally it takes 2 to 3 weeks for this process to be completed.

Liquefaction necrosis: Infected brain within the capsule undergoes liquefactive necrosis with eventual formation of pus. Accumulation of pus cause enlargement of the abscess.

Stage of rupture: Enlargement of the abscess eventually leads to rupture of the capsule containing the abscess and this material finds its way into the cerebrospinal fluid as shown in the above diagram.

Cerebellar abscess which occupy the posterior fossa cause raised intra cranial tension earlier than those above the tentorium. This rapidly raising intra cranial pressure cause coning or impaction of the flocculus or brain stem into the foramen magnum. Coning produces impending death. If the walling off process (development of capsule) is slow, softening of brain around the developing abscess may allow spread of infection into relatively avascular white matter, leading to the formation of seconday abscesses separate from the original or connected to the original by a common stalk. This is how multilocular abscesses are formed. Eventually the abscess may rupture into the ventricular system or subarachnoid space, causing meningitis and death.

The mortality rate of brain abscess is around 40%, early diagnosis after the advent of CT scan has improved the prognosis of this disease considerably..

The bacteriological flora is usually a mixture of aerobes and obligate anaerobes. Anaerobic streptococci are the commonest organisms involved. Pyogenic staphylococci is common in children. Gram negative organims like proteus, E coli and Pseudomonas have also been isolated.

Clinical features:

The earliest stage where the brain tissue is invaded (stage of encephalitis) is marked by the presence of headache, fever, malaise and vomiting. Drowsiness eventually follow. These early features may be masked by the complications such as meningitis or lateral sinus thrombosis. If this stage progresses rapidly to generalised encephalitis before it could be contained by the formation of the capsule, drowsiness may progress to stupor and coma followed by death.. Usually the period of local encephalitis is followed by a latent period during which the pus becomes contained within the developing fibrous capsule. During this latent phase the patient may be asymptomatic.

During the next state (stage of expansion) the enlarging abscess first cause clinical features due to the alteration of CSF dynamics, and site specific features may also be seen due to focal neurological impairement. The pulse rate slows with rising intracranial pressure, the temperature may fall to subnormal levels. Drowsiness may alternate with periods of irritability. Papilloedema is also found due to elevated CSF pressure.

Clinical features also vary according to the site of involvement. Hence the differences that are seen between the cerebral and cerebellar abscess.

Cerebral (Temporo sphenoidal abscess):

A cerebral abscess in the dominant hemisphere often cause nominal aphasia, where in the patient has difficulty in naming the objects which are in day to day use. He clearly knows the function of these objects. Visual field defects arise from the involvement of optic radiations. Commonly there is quadrantic homonymous hemianopia, affecting the upper part of the temporal visual fields, more rarely it may also involve the lower quadrants. The visual field loss are on the side opposite to that of the lesion. This can be assessed by confrontation method. Upward development affects facial movements on the opposite side, and then progressively paralysis of the upper and lower limbs. If the expansion occur in inward direction then paralysis first affects the leg, then arm and finally the face.

Cerebellar abscess:

The focal features associated with cerebellar abscess is weakness and muscle incoordination on the same side of the lesion. Ataxia causes the patient to fall towards the side of the lesion. Patient may also manifest intention tremors which may become manifest by the finger nose test. This test is performed by asking the patient to touch the tip of the nose with the index finger first with the eyes open and then with the eyes closed. The patient may often overshoot the mark when attempted with the eyes closed in case of cerebellar abscess. The patient may also have spontaneous nystagmus. Dysdiadokinesis is also positive in these patients.

Investigations:

CT scan and MRI scans are the present modes of investigation. Scan is ideally performed using contrast media. These scans not only reveal the position and size of the abscess, the presence of localised encephalitis can be distinguished from that of an encapsulated abscess. Associated conditions such as subdural abscess, and lateral sinus thrombosis can also be seen.

Management:

Surgical drainage of the abscess, followed by mastoidectomy to clear the ear disorder.