LOCALISED NEUROLOGICAL DISEASE AND ITS MANAGEMENT A. INTRACRANIAL

SECTION IV LOCALISED NEUROLOGICAL DISEASE AND ITS MANAGEMENT A. INTRACRANIAL



HEAD INJURY





FOCAL DAMAGE







Tentorial/tonsillar herniation (syn. ‘cone”)


It is unlikely that high intracranial pressure alone directly damages neuronal tissue, but brain damage occurs as a result of tonsillar or tentorial herniation (see page 81). A progressive increase in intracranial pressure due to a supratentorial haematoma initially produces midline shift. Herniation of the medial temporal lobe through the tentorial hiatus follows (lateral tentorial herniation), causing midbrain compression and damage. Uncontrolled lateral tentorial herniation or diffuse bilateral hemispheric swelling will result in central tentorial herniation. Herniation of the cerebellar tonsils through the foramen magnum (tonsillar herniation) and consequent lower brain stem compression may follow central tentorial herniation or may result from the infrequently occurring traumatic posterior fossa haematoma.





DIFFUSE DAMAGE








HEAD INJURY – CLINICAL ASSESSMENT




PETROUS FRACTURE


Bleeding from the external auditory meatus or CSF otorrhoea:




3. Conscious level – Glasgow Coma Score (GCS)


Assess patient’s conscious level in terms of eye opening, verbal and motor response on admission (see page 5) and record at regular intervals thereafter. An observation chart incorporating these features is essential and clearly shows the trend in the patient’s condition. Deterioration in conscious level indicates the need for immediate investigation and action where appropriate.



Note: This chart shows a ‘14 point scale’ with a maximum score of ‘14’ in a fully conscious patient. Many centres use a 15 point coma scale where ‘Flexion to pain’ is divided into ‘normal’ or ‘spastic’ flexion (see page 29).



4. Pupil response


The light reflex (page 142) tests optic (II) and oculomotor (III) nerve function. Although II nerve damage is important to record and may result in permanent visual impairment, it is the III nerve function which is the most useful indicator of an expanding intracranial lesion. Herniation of the medial temporal lobe through the tentorial hiatus may damage the III nerve directly or cause midbrain ischaemia, resulting in pupil dilatation with impaired or absent reaction to light. The pupil dilates on the side of the expanding lesion and is an important localising sign. With a further increase in intracranial pressure, bilateral pupillary dilatation may occur.




5. Limb weakness


Determine limb weakness by comparing the response in each limb to painful stimuli (page 30). Hemiparesis or hemiplegia usually occurs in the limbs contralateral to the side of the lesion. Indentation of the contralateral cerebral peduncle by the edge of the tentorium cerebelli (Kernohan’s notch) may produce an ipsilateral deficit, a false localising sign more often seen with chronic subdural haematomas. Limb deficits are therefore of limited value in lesion localisation.







HEAD INJURY – INVESTIGATION AND REFERRAL CRITERIA



IN THE ACCIDENT AND EMERGENCY DEPARTMENT (A&E)


Various guidelines now exist. The following are based on those from the National Institute for Health and Clinical Excellence (NICE). (Further details available at http://www.nice.org.uk).












Admit to Hospital Discharge from A&E















HEAD INJURY – MANAGEMENT


Management aims at preventing the development of secondary brain damage from intracranial haematoma, ischaemia, raised intracranial pressure with tentorial or tonsillar herniation and infection.












INTRACRANIAL HAEMATOMA


Most intracranial haematomas require urgent evacuation – evident from the patient’s clinical state combined with the CT scan appearance of a space-occupying mass.






TREATMENT OF RAISED INTRACRANIAL PRESSURE (ICP)


Raised ICP in the absence of any easily treatable condition (e.g. intracranial haematoma or raised pCO2) requires careful management. The various techniques used to lower ICP have already been described (pages 83–84) but these must not be applied indiscriminately.


Recent studies show that even in a modern ITU head injured patient are still at risk of sustaining potentially harmful “insults” to the brain in the first few days after head injury from high ICP, low BP, low cerebral perfusion pressure (CPP), hypoxaemia, hypoglycaemia or raised temperature.


Most believe that both raised ICP and reduced cerebral perfusion pressure (CPP) can exacerbate brain damage. What is less clear is whether treatment should focus on lowering ICP or increasing CPP. When autoregulation is impaired, raising CPP beyond 70 mmHg could cause harm. The blind use of hyperventilation in the past to lower ICP by causing vasoconstriction and reduced intracranial blood volume has now been recognised to produce worse outcomes by aggravating cerebral ischaemia.


Patient selection for ICP monitoring: Monitoring ICP and CPP is most relevant in patients with a flexion response to painful stimuli or worse (a response of ‘localising to pain’ signifies a milder degree of injury and spontaneous recovery is likely). Such patients may have already undergone removal of an intracranial haematoma or may have had no mass lesion on CT scan (i.e.: diffuse injury or contusional damage). Each neurosurgical unit is likely to have its own policy for ICP monitoring but the following outline may serve as a guide for patients with no intracranial mass lesion –






DEPRESSED SKULL FRACTURE


This injury is caused by a blow from a sharp object. Since diffuse ‘deceleration’ damage is minimal, patients seldom lose consciousness.




COMPOUND DEPRESSED FRACTURE (open injury)


A scalp laceration is related to (but does not necessarily overlie) the depressed bone segments. A compound depressed fracture with an associated dural tear may result in meningitis or cerebral abscess.






DELAYED EFFECTS OF HEAD INJURY




CEREBROSPINAL FLUID (CSF) LEAK


After head injury a basal fracture may cause a fistulous communication between the CSF space and the paranasal sinuses or the middle ear. Profuse CSF leaks (rhinorrhoea or otorrhoea) are readily detectable, but brain may partially plug the defect and the leak may be minimal or absent. Patients risk developing meningitis particularly in the first week, but in some this occurs after several years. When this is associated with anterior fossa fractures, it is usually pneumococcal; when associated with fractures through the petrous bone, a variety of organisms may be involved.


Clinical signs of a basal fracture have previously been described (page 222). The patient may comment on a ‘salty taste’ in the mouth. Anosmia suggests avulsion of the olfactory bulb from the cribriform plate.









OUTCOME AFTER SEVERE HEAD INJURY


Head injury remains a major cause of disability and death, especially in the young. Of those patients who survive the initial impact and remain in coma for at least 6 hours, approximately 40% die within 6 months. The extent of recovery in the remainder depends on the severity of the injury. Residual disabilities include both mental (impaired intellect, memory and behavioural problems) and physical defects (hemiparesis and dysphasia). Most recovery occurs within the first 6 months after injury, but improvement may continue for years. Physiotherapy and occupational therapy play an important role not only in minimising contractures and improving limb power and function but also in stimulating patient motivation.


Outcome is best categorised with the Glasgow Outcome Scale (GOS – see page 214) which uses dependence to differentiate between intermediate grades. After severe injury, about 40% regain an independent existence and may return to premorbid social and occupational activities. Inevitably some remain severely disabled requiring long term care, but few (< 2%) are left in a vegetative state with no awareness or ability to communicate with their environment (see page 214). Prognosis in this group is marginally better than for non-traumatic coma – with about one-third of those vegetative at one month regaining consciousness within one year; of those who regain consciousness, over two-thirds either subsequently die or remain severely disabled. Of those vegetative at 3 months after the injury, none regain an independent existence.





CEREBROVASCULAR DISEASES


Vascular diseases of the nervous system are amongst the most frequent causes of admission to hospital. The annual incidence in the UK varies regionally between 150–200/100 000, with a prevalence of 600/100 000 of which one-third are severely disabled.


Better control of hypertension, reduced incidence of heart disease and a greater awareness of all risk factors have combined to reduce mortality from stroke. Despite this, stroke still ranks third behind heart disease and cancer as a cause of death in affluent societies.



RISK FACTORS


Prevention of cerebrovascular disease is more likely to reduce death and disability than any medical or surgical advance in management. Prevention depends upon the identification of risk factors and their correction. Increasing age is the strongest risk factor (but is not amenable to correction).














OCCLUSIVE AND STENOTIC CEREBROVASCULAR DISEASE



PATHOLOGY


The normal vessel wall comprises:



Within brain and spinal cord tissue the adventitia is usually very thin and the elastic lamina between media and adventitia less apparent.


The intima is an important barrier to leakage of blood and constituents into the vessel wall. In the development of the atherosclerotic plaque, damage to the endothelium of the intima is the primary event.






CLINICAL SYNDROMES – LARGE VESSEL OCCLUSION


OCCLUSION OF THE INTERNAL CAROTID ARTERY – may present in a ‘stuttering’ manner due to progressive narrowing of the lumen or recurrent emboli.


The degree of deficit varies – occlusion may be asymptomatic and identified only at autopsy, or a catastrophic infarction may result.




The origins of the vessels from the aortic arch are such that an innominate artery occlusion will result not only in the clinical picture of carotid occlusion but will produce diminished blood flow and hence blood pressure in the right arm.



The outcome of carotid occlusion depends on the collateral blood supply primarily from the circle of Willis, but, in addition, the external carotid may provide flow to the anterior and middle cerebral arteries through meningeal branches and retrogradely through the ophthalmic artery to the internal carotid artery.




Jul 16, 2016 | Posted by in NEUROSURGERY | Comments Off on LOCALISED NEUROLOGICAL DISEASE AND ITS MANAGEMENT A. INTRACRANIAL

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