Routine blood test: visible WBC mild↑

Cerebrospinal fluid routine: normal/mild pressure↑, nucleated cell count↑ (mainly lymphocytes), protein mild to moderate↑, sugar/chloride normal

Cerebrospinal fluid etiology: detection of HSV-specific antibodies, HSV-DNA

CT: Focal abnormalities (low-density lesions in the frontotemporal region on one/both sides); however, there may be no abnormal findings on CT within the first 4 to 5 days after the onset of HSE symptoms.

MRI: early diagnosis, showing diseased areas

EEG: Diffuse high-amplitude slow waves (especially in the frontotemporal region)

Brain biopsy: the gold standard for diagnosis

Asymptomatic type

symptomatic

Increased volume of the brain tissue itself (cerebral edema → vasogenic, cytotoxic, mixed), increased cerebral blood flow, excessive cerebrospinal fluid, intracranial space-occupying lesions, and narrow cranial cavity

Compensation stage (8~10% compensation volume) → early stage (non-localizing symptoms, Cushing reaction) → peak stage (scattered infarcts in the brain, signs of herniation, scattered Cushing reaction) → late stage (depletion stage)

General symptoms (non-localized symptoms): three main signs of increased intracranial pressure - headache, vomiting, and papilledema

secondary symptoms

Focal symptoms (localizing symptoms): focal epilepsy/symptomatic epilepsy, paralysis (especially upper motor neuron paralysis of one limb), visual disturbances, psychiatric symptoms

Presumptive localization symptoms

Cushing reaction/systemic vasopressor reflex: acute increase in intracranial pressure causes blood pressure↑, heart rate↓, and respiratory slowdown; physiological significance: can increase cerebral perfusion, increase blood oxygen content, and improve cerebral hypoxia

Macewen Sign: Broken Can Sound

Symptoms gradually worsen and neurological signs are superimposed

Headache, vomiting, papilledema

Cerebral cortex: slightly

corpus callosum

ventricular system

Thalamus: Symptoms are relatively subtle, most of them only have headaches; mental symptoms, obesity, and polyuria may be present

Basal ganglia: sensory impairment, hemiparesis, involuntary movements, ataxia, nystagmus

Brainstem: Different levels can produce different localization symptoms

cerebellum

Cerebellopontine angle: vertigo, tinnitus, progressive hearing loss, nystagmus, cerebellar signs

Intrasellar/suprasellar: early typical manifestations are endocrine disorders; after enlargement, there may be temporal hemianopia in both eyes.

Parasellar/clival: early typical manifestation is unilateral cranial nerve palsy (especially V and VI cranial nerves)

It is more common in children and adolescents; early symptoms include fever, chills, headache, general weakness, drowsiness and fatigue, with further symptoms of focal nerve localization and intracranial hypertension appearing 1 to 2 weeks later.

Acute fulminant type: sudden onset, early coma, and high mortality; severe diffuse suppurative encephalitis can be seen at autopsy, and the abscess capsule may not be formed or may be partially formed.

Meningitis type: Mainly purulent meningitis (because the superficial location of the abscess causes severe inflammation in the adjacent subarachnoid space, masking the symptoms of the brain abscess itself)

Brain tumor type: The brain abscess capsule is intact, the surrounding edema has subsided, and the disease develops slowly

Hybrid

Occult type: There is no clear history of infection, surgical treatment is only performed because of intracranial space-occupying lesions, and the diagnosis is only made during the operation.

The lesion is located in or near the ventricular system, causing obstruction of the ventricles and inability to communicate with the subarachnoid space.

The ventricles and subarachnoid space remain patent

More common in congenital aqueduct occlusion

Mainly manifested by increased intracranial pressure

Normal pressure hydrocephalus: progressive dementia without signs of increased intracranial pressure, difficulty starting, urinary incontinence