Clinical syndromes

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Clinical presentation of spontaneous ICH depends on site and size. Therefore, clinical investigation as well as neuroimaging are both important for a reliable diagnosis. All attempts to make a probabilistic diagnosis on clinical grounds alone to differentiate between ischemic and hemorrhagic stroke have not been considered satisfactory [45].

In our series of 1539 ICH cases we have located 45% in the putaminal region and in the thalamus, 34% in a lobar location, 5% in the cerebellum, about 4% in the pons, and 11% were not classifiable (Table 10.1).

Putaminal hemorrhages are the most frequent ones. If the hemorrhage spreads from the putamen into the thalamic region, they are called putaminotha-lamic. Then they show a large volume extending over the area of the basal ganglia and deep white matter of one hemisphere. Such an ICH can rupture into the lateral or third ventricles, giving rise to sudden posturing and coma. More often, progression is not abrupt but gradual and can be seen occurring over several hours, showing an increase of sensorimotor hemiparesis and a gradual decrease of alertness. Usually transition into drowsiness and stupor occurs in parallel with a decrease in motor function. If a progressive deterioration of consciousness is seen in a hemiparetic patient with a sensorimotor hemipar-esis, this can give rise to suspicion of a growing hematoma. Noting such a progression is vital and contrasts with ischemic strokes, most of which tend to remain stable. If no deterioration or progression occurs in the first hours or days, hemorrhages such as small or medium-sized putaminal bleedings also tend to remain stable after the first few days and cannot be distinguished from ischemic infarcts in the basal ganglia and capsular region on clinical grounds alone. They both present with sudden onset of sensorimotor hemiparesis of varying degree and can both be associated with additional hemispheric symptoms such as aphasia or neglect. This contradicts the prevailing opinion at some centers that "typical" hemiparetic strokes that remain stable can be reliably considered to be caused by ischemia and therefore do not need confirmation with neuroimaging. In general, there is also no medical rationale to restrict imaging to young patients or to patients with some other demographic or clinical feature.

ICH can also occur extremely abruptly and loss of consciousness can occur within minutes after onset. This is the case in large putaminal or thalamic hematomas that rupture into the ventricles, or in pontine hemorrhages extending over the midline.

Contralateral limb weakness and hemisensory symptoms are typical of mid-sized putaminal hemorrhages, whereas bleeding into the thalamus causes a distinct and total hemisensory loss and dense hemiplegia.

Conjugate eye deviation to the side of the bleeding signals extension into the frontal lobe. This is a sign either of frontal lobar hemorrhage or of a putaminal hemorrhage extending into the deep frontal white matter. In contrast, thalamic hemorrhage can be accompanied by a conjugate spasm of both eyes, appearing as convergent downward gaze (the patient looks at his/her nose tip). The pupil which is smaller denotes the hemispheric side of the bleeding, and, when present, this invariably denotes involvement of subthalamic structures. Such cases have to be monitored closely because of the likelihood of rupture into the ventricles. This is the case when sudden, bilateral localizing signs appear and loss of consciousness is the rule.

Vomiting is a frequent sign of ICH but can also indicate ischemic stroke. It can be a prominent sign in posterior fossa hemorrhage, and, although patients with cerebellar hemorrhages almost always vomit

early in the clinical course, it is not a reliable sign with either localizing or etiological value. Many patients with posterior fossa hemorrhage show severe impairment of sitting balance and ataxia that can be pronounced ipsilaterally. Close observation of vital parameters is crucial, as deterioration can be sudden or progressive over the first few days after onset. Evacuation of the hematoma can also become necessary after some days.

Contrasting with lay beliefs, headache is also not a cardinal symptom of ICH. Headache can occur in large hematomas and has no localizing value unless it is very severe and then indicates rupturing in cerebrospinal fluid space. In patients with loss of consciousness meningeal irritation must not be apparent.

Clinical presentation of spontaneous ICH depends on site and size. The most frequent putaminal hemorrhages show a sudden onset. Progressive deterioration of consciousness points to a growing hematoma, and sudden posturing and coma to a rupture of the bleeding into the lateral or third

Figure 10.3. CT: large putaminothalamic hemorrhage with rupture into lateraland third ventricles. The estimated blood volume is 60 ml.

Figure 10.1. CT: smallputaminalhemorrhage (possibly secondary to ischemic infarction).

Figure 10.3. CT: large putaminothalamic hemorrhage with rupture into lateraland third ventricles. The estimated blood volume is 60 ml.

Figure 10.1. CT: smallputaminalhemorrhage (possibly secondary to ischemic infarction).

Figure 10.2. MRI: subacute thalamic hemorrhage with gradient echo (GRE) sequence (left).

Figure 10.4. MRI: lobar hematoma in the left temporal lobe.

ventricle. Vomiting and headache are frequent, but not reliable, signs. See Figures 10.1-10.6.

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