Without further ado, let's get straight to the point

1. Putamen and basal ganglia hemorrhage

It is the most common site of hypertensive intracerebral hemorrhage, often affecting the internal capsule. Patients typically present with head and eyes turning toward the side of the bleeding lesion, showing "gaze toward the lesion" and "three hemi" symptoms: hemiplegia, hemisensory impairment, and hemianopia. There is contralateral limb paralysis to the hemorrhage, with early-stage decreased or absent muscle tone and tendon reflexes in the paralyzed limb, followed by gradual escalation - upper limb flexion, lower limb extension, hyperactive tendon reflexes, ankle clonus, and positive pathological reflexes, representing a classic upper motor neuron hemiplegia. Contralateral sensory impairment is present with absent or delayed response to pinprick stimulation of limbs and face. If the patient is conscious and cooperative during examination, contralateral hemianopia may also be detected. When the hematoma ruptures into the lateral ventricle, or even fills the entire lateral ventricle (lateral ventricular cast), the prognosis is poor.

2. Pontine Hemorrhage

It often has abrupt onset, progressing to deep coma within minutes with critical condition. Pontine hemorrhage usually starts from one side and rapidly spreads bilaterally, causing bilateral limb paralysis (most cases being flaccid, few showing spasticity or decorticate rigidity). Both sides show positive pathological reflexes. Pupils become extremely constricted ("pinpoint pupils"). Due to these characteristic signs, some patients may present with central hyperventilation and typically die within 1-2 days.

3. Cerebellar Hemorrhage

Mildly affected patients remain conscious and often complain of severe occipital headaches, dizziness, vomiting, slurred speech, and nystagmus. Their limbs show no paralysis, but affected-side ataxia is present. When the hematoma gradually ruptures into the fourth ventricle, it may cause acute hydrocephalus. Severe occipital herniation can lead to sudden coma, irregular breathing or even respiratory arrest, ultimately resulting in death from respiratory and circulatory failure.

4. Subcortical hemorrhage in the cerebral lobes

Symptoms are related to hematoma size, typically including headache, vomiting, photophobia, and irritability. Corresponding neurological deficits in the affected cerebral lobe are also prominent. As the hematoma expands, symptoms of increased intracranial pressure become evident.

5. Thalamic hemorrhage

Upon onset, most patients experience coma and hemiplegia. Those with medial or inferior thalamic hemorrhage may present with typical ocular signs: vertical gaze palsy (predominantly upward gaze impairment) with eyes converging inward toward the nose; ocular deviation downward and medially toward the side of hemorrhage; miotic and unequal pupils with sluggish light reflex; impaired convergence and gaze fixation. External expansion of hemorrhage affecting the internal capsule manifests as the "three hemi-syndromes". Ventricular extension of thalamic hemorrhage worsens the condition, causing high fever and tonic limb convulsions while increasing the incidence of cerebral-visceral syndrome.

6. Subcortical hemorrhage (lobar hemorrhage)

This ranks second in incidence after basal ganglia hemorrhage. Similar to thalamic hemorrhage, clinical manifestations vary by primary bleeding site. Most scholars observe predominant involvement in the parietal, temporal and occipital lobes (posterior cerebrum), differing clinically from basal hemorrhage. Lobar hemorrhages readily rupture into adjacent subarachnoid spaces but remain distant from midline structures, rarely extending into ventricular systems. Patients exhibit marked meningeal irritation but milder consciousness impairment, generally demonstrating better prognosis. Characteristic clinical features include:

(1) Rare and relatively mild consciousness disturbance.

%% (2) Hemiplegia and conjugate gaze palsy occur less frequently and are milder in severity because lobar hemorrhages do not typically involve the internal capsule as readily as basal ganglia hemorrhages.

(3) Meningeal irritation is more commonly observed.

(4) Occipital lobe hemorrhage may present with transient amaurosis and cortical blindness; temporoparietal lobe hemorrhage with homonymous hemianopia and mild hemiplegia; dominant hemisphere involvement may cause aphasia; while frontal lobe hemorrhage may manifest as intellectual impairment, urinary incontinence, and mild hemiplegia.

7. Intraventricular hemorrhage

Primary intraventricular hemorrhage is rare, with most cases being secondary to thalamic hemorrhage or basal ganglia hemorrhage. The clinical manifestations of these patients are closely related to the primary bleeding site, hematoma volume, and extent of ventricular involvement. The closer the primary bleeding site is to the ventricles, the more likely the hemorrhage will extend into and invade the ventricles. Consequently, patients with intraventricular hemorrhage experience more severe conditions. Clinically, in addition to the symptoms and signs of the primary lesion, there are manifestations of brainstem involvement and rapid increases in intracranial pressure.