Herpes Simplex Encephalitis

Herpes simplex encephalitis (HSE), overwhelmingly caused by HSV-1 in adults (HSV-2 is a more common cause in neonates, typically from perinatal transmission, see Neonatal Meningitis entry), is the most common cause of sporadic, severe viral encephalitis in immunocompetent individuals.

Itresults from either primary infection with direct neural spread, or, more commonly in adults, reactivation of latent virus within the trigeminal ganglion with retrograde spread, characteristically causing a necrotizing, hemorrhagic inflammation with a strong predilection for the temporal and inferior frontal lobes.

Untreated, mortality approaches 70%, making rapid recognition and empirical treatment before confirmatory testing genuinely essential rather than a stylistic preference.

Fever, headache, and altered mental status are near-universal, but the more specific and diagnostically important features reflect the temporal lobe predilection: behavioral and personality change, olfactory or gustatory hallucinations, anomia and other focal aphasic features, and focal or generalized seizures (occurring in roughly half of cases, sometimes as the presenting feature).

Focal neurological deficits (hemiparesis, cranial nerve palsies) may develop as the disease progresses.

The clinical picture can evolve rapidly over days, and any patient with fever, altered consciousness, and new focal neurological or behavioral features should prompt urgent consideration of this diagnosis.

CSF HSV PCR is the diagnostic test of choice, with high sensitivity and specificity, though a false negative result is possible very early in the illness course (within the first 24 to 48 hours), and a repeat lumbar puncture and PCR after 3 to 7 days should be performed if clinical suspicion remains high despite an initial negative result
CSF typically shows a lymphocytic pleocytosis, elevated protein, and normal or mildly reduced glucose; red blood cells or xanthochromia may be present reflecting the hemorrhagic, necrotizing nature of the inflammation, an important supportive clue
MRI brain is the imaging investigation of choice, showing characteristic asymmetric T2/FLAIR hyperintensity involving the medial temporal lobes, insula, and inferior frontal lobes, often with associated hemorrhage; CT is far less sensitive, particularly early in the disease course, and a normal CT should never be used to defer treatment or lumbar puncture
EEG may show characteristic periodic lateralized epileptiform discharges (PLEDs) over the temporal region, supporting the diagnosis where imaging or CSF findings are equivocal

IV aciclovir 10 mg/kg every 8 hours (adjusted for renal function), started empirically on clinical suspicion, without waiting for confirmatory PCR or imaging, given the dramatic mortality difference between early and delayed treatment; this is one of the clearest examples in infectious disease medicine where empirical treatment before diagnostic confirmation is the standard of care rather than an exception to it
Adequate hydration is essential during aciclovir administration given the risk of crystal nephropathy, and renal function should be monitored
Treatment duration is typically 14 to 21 days (21 days generally preferred given evidence of reduced relapse with the longer course compared with historically shorter regimens), with some specialists repeating CSF PCR near the end of treatment to confirm viral clearance before stopping, particularly in more severe or complicated cases
Supportive care includes management of raised intracranial pressure if present, seizure control (levetiracetam or another appropriate anticonvulsant), and, in severe cases, ICU level supportive care and ventilatory support
If aciclovir is stopped after negative PCR results but the patient fails to improve or worsens, reconsideration of the diagnosis (including a repeat lumbar puncture and PCR, and broadening the differential to other causes of encephalitis) is essential, given the possibility of an early false negative result or an alternative diagnosis
Neuropsychological and cognitive assessment, along with rehabilitation input, is important during recovery given the significant risk of persistent memory and behavioral sequelae even with prompt treatment, reflecting the vulnerability of the temporal lobe structures affected

Referral: neurology and infectious disease input for all suspected cases; ICU for significant reduction in consciousness, status epilepticus, or evolving raised intracranial pressure; neuropsychology and rehabilitation services during recovery.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Bell's Palsy

Also known as: Facial palsy

Acute, idiopathic, unilateral peripheral facial nerve (CN VII) palsy, presumed due to viral reactivation (most implicated: HSV-1, also VZV) causing inflammation, edema, and compression of the nerve within the narrow bony facial canal (labyrinthine segment is narrowest point).

Most common cause of acute facial paralysis (~60–75% of cases).

Diagnosis of exclusion.

Classified by:

Not formally subtyped, but distinguished by grading of severity ; House-Brackmann scale (Grade I normal to Grade VI complete paralysis) ; used for prognostication and monitoring recovery
Distinguish from other causes of facial palsy grouped as: idiopathic (Bell's palsy), infectious (Ramsay Hunt/VZV, Lyme disease, otitis media, HIV), traumatic, neoplastic (parotid tumor, cerebellopontine angle tumor, facial nerve schwannoma), other (Guillain-Barré, sarcoidosis, diabetes mellitus, pregnancy ; increased incidence in 3rd trimester/postpartum)

Acute onset (hours to 1–2 days), unilateral, peaks within 72 hours
Lower motor neuron pattern; critical distinguishing feature: entire hemiface affected including forehead (unlike UMN/stroke lesions which spare the forehead due to bilateral cortical innervation of frontalis)
Inability to raise eyebrow, close eye (lagophthalmos), flatten nasolabial fold, purse lips/smile on affected side
Bell's phenomenon: upward eye deviation on attempted closure (normal reflex, becomes visible due to lagophthalmos)
Associated symptoms (reflect involvement of nerve branches proximal to the lesion):
Hyperacusis (stapedius nerve branch)
Loss of taste anterior 2/3 tongue (chorda tympani)
Decreased tearing or, paradoxically, excessive tearing (greater petrosal nerve/impaired drainage due to weak orbicularis oculi)
Postauricular/ear pain (often precedes palsy by 1-2 days)
Numbness/heaviness sensation on affected side (subjective, sensory exam usually objectively normal ; true sensory loss suggests alternative diagnosis)
Red flags suggesting alternative diagnosis (NOT Bell's palsy):
Gradual onset over weeks (suggests tumor ; parotid mass, acoustic neuroma, cholesteatoma)
Bilateral facial weakness (Guillain-Barré, sarcoidosis, Lyme disease, bilateral Bell's is rare)
Vesicles in ear canal/pinna/palate (Ramsay Hunt syndrome; VZV reactivation, worse prognosis)
Other cranial neuropathies or limb weakness/ataxia (brainstem stroke, tumor)
Parotid mass or facial twitching preceding palsy (parotid malignancy)
Recurrent ipsilateral or alternating palsy (consider sarcoidosis, tumor)
History of tick exposure/erythema migrans rash/endemic area (Lyme disease)

Clinical diagnosis; no routine investigations needed in typical presentation with no red flags.

Investigate selectively if atypical features present:

MRI brain with contrast (internal auditory canal/cerebellopontine angle protocol): if gradual onset, bilateral, other neurological signs, or no improvement/worsening after 3–4 months ; excludes tumor, stroke, MS
Lyme serology: if endemic area, tick exposure, rash, bilateral palsy
VZV serology/PCR if vesicles present (Ramsay Hunt)
Blood glucose/HbA1c: diabetes associated with higher incidence and poorer recovery
Electrodiagnostic testing (electroneurography/EMG): if complete paralysis, to help predict prognosis and guide surgical decompression discussion (rarely used)

Differentials: stroke (UMN pattern ; forehead spared; other neuro deficits), Ramsay Hunt syndrome, Guillain-Barré syndrome (bilateral, ascending weakness, areflexia), Lyme disease, acoustic neuroma/CPA tumor, parotid malignancy, otitis media/mastoiditis, multiple sclerosis, sarcoidosis (bilateral, uveoparotid fever), HIV, trauma (temporal bone fracture).

Eye protection; mandatory, prevents exposure keratopathy/corneal ulceration (most important preventable complication):
Artificial tears (lubricating drops) hourly while awake
Lubricating ointment + eye patch/taping shut at night
Wraparound sunglasses during day
Corticosteroids ; first-line, most benefit if started within 72 hours of onset:
Prednisolone 50–60mg PO od for 10 days (or 60mg for 5 days then taper over 5 days); improves rate and completeness of recovery
Antivirals; adjunct, evidence weaker alone but often combined with steroids, especially in severe palsy (House-Brackmann IV–VI) or suspected Ramsay Hunt:
Aciclovir 400mg 5x/day for 7–10 days, or valaciclovir 1g PO tds for 7 days
For confirmed Ramsay Hunt: valaciclovir + prednisolone, higher-dose regimens sometimes used
Analgesia for associated pain (paracetamol, NSAIDs)
Facial physiotherapy: may help, particularly for synkinesis prevention in moderate-severe cases; evidence modest
Surgical decompression: rarely indicated, reserved for cases with >90% degeneration on electroneurography within 2 weeks and no voluntary motor unit potentials on EMG; controversial, specialist ENT/neurosurgical decision

Prognosis: ~70% recover fully without treatment; treatment improves this further. Most improvement begins within 3 weeks; full recovery typically by 3–6 months. Poor prognostic factors: complete paralysis at onset, older age, diabetes, hyperacusis, severe pain, delayed treatment initiation.

Complications if untreated/severe: exposure keratopathy, corneal ulceration, synkinesis (aberrant reinnervation causing involuntary movements), crocodile tears syndrome (gustatory lacrimation), persistent weakness (~15–30% incomplete recovery in untreated cases).

Referral: ophthalmology if corneal complications; ENT/neurology if atypical features, no improvement by 3–4 months, or recurrent/bilateral palsy.

Herpes Simplex Encephalitis

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management