Question 6

Compare and contrast the clinical manifestations, aetiology, treatment and complications of posterior reversible encephalopathy syndrome (PRES) with herpes simplex virus (HSV) encephalitis

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College answer


HSV encephalitis

Clinical manifestations (4 marks)

The symptoms of PRES evolve rapidly over hours to days

Hypertension is frequent but not invariable. The hypertensive crisis may precede the neurologic syndrome by 24 hours or longer.

The clinical syndrome of PRES is characterized by

  • headaches
  • altered consciousness ranges from mild somnolence to coma
  • visual disturbances
  • seizures – Seizures are often the presenting manifestation

Rarely patients can have symptoms referable to the upper cervical spinal cord (limb weakness, bladder dysfunction), along with one or more of the symptoms above.

Focal     neurologic    findings               are usually acute - <1 week in duration

- and include

  • altered mentation and level of consciousness
  • focal cranial nerve deficits
  • hemiparesis
  • dysphasia, aphasia
  • ataxia
  • focal seizures

The majority of patients will have one of the above symptoms plus fever

Aetiology (1 mark)

  • Hypertension
  • Immunosuppressive therapy eg. cyclosporine
  • Renal disease
  • Autoimmune disorders
  • sepsis


Management (3 marks)

  • reduction in BP, especially diastolic BP to 100/110
  • Discontinuation of cytotoxic
  • Seizure therapy
  • Organ failure therapy
  • - in the peripartum setting treat as for eclampsia

IV acyclovir


(2 marks)

  • ischemia
  • Intracranial haemorrhage
  • death
  • Neurological deficit ranging from severe to mild

-Behavioural abnormalities


- cognitive impairment



Though the college must be commended for their lucid tabulated answer, the inclusion of "death" in the complications deserves a raised eyebrow (because surely that can't have attracted a grade if the trainees wrote it). Also, just putting "HSV" under the "aetiology" heading would have probably attracted comments like "insufficient knowledge and detail"

Anyway, the specific information regarding HSV encephalitis is derived from by Bradshaw & Ventakesan (2016) for HSV, and Walter Bartynski (Part 1 or Part 2, 2008) for PRES.

PRES vs. HSV encephalitis
HSV encephalitis PRES
Pathophysiology / aetiology
  • Viral illness
  • Transmitted along an axon from the ganglion of the trigeminal nerve, where it lays dormant
  • Pathophysiology is inflammatory and (Bradshaw et al, 2016)
  • Characterised by the development of inflammatory cerebral oedema 
  • Exhibits tropism for the orbitofrontal and mesiotemporal lobe
  • Hypertensive disorder
  • Hypertension, followed by failed autoregulation, followed by hyperperfusion
  • As the result of hypertension, permeability of cerebral vessels increases
  • Vasogenic cerebral oedema results
Clinical manifestations

Historical features and symptoms
(Sili et al, 2014)

  • Subacute course (>24 hrs)
  • Headache
  • Altered mental status initially
  • Abnormal behaviour
  • Progressively worsening level of consciousness

Features on examination

  • Focal signs are possible
  • Fever
  • Seizures

CSF biochemistry

  • CSF pleocytosis,
    mainly lymphocytic
  • Elevated CSF protein
  • HSV PCR positive


  • Contrast-enhancing lesions on MRI
  • Evidence of lost grey-white differentiation on CT
  • EEG findings (non-pathognomic)

Historical features and symptoms

  • Headache
  • Visual disturbance
  • Altered mental status

Features on examination

  • Blindness
  • Hypertension
  • Seizures

CSF biochemistry (Ellis, 2019)

  • CSF pleocytosis
  • Mildly elevated protein


  • MRI evidence of oedema
  • Oedema is symmetric (bilateral)
  • Posterior occipital or parietal distribution (but this is not essential): in fact three major anatomical patterns of distribution exist:
    • holohemispheric
    • superior frontal sulcal
    • primary parietal-occipital
  • Nonspecific EEG findings
  • IV aciclovir 10 mg/kg q8h for 14–21 days
  • Foscarnet is a second option
  • Aggressive control of blood pressure
  • Give antiepileptics if seizures were a presenting problem.
  • Stop the causative drug or arrest the causative process (eg. eclampsia)
  • Decreased level of consciousness
  • Seizures, status epilepticus
  • Development of NMDA receptor antibodies

Hypertensive complications (Fischer et al, 2017)

  • Intracranial haemorrhage (eg subarachnoid or intraparenchymal)
  • Status epilepticus

Persistent neurological sequelae are rare

Persisting epilepsy may occur


Staykov, Dimitre, and Stefan Schwab. "Posterior reversible encephalopathy syndrome." Journal of Intensive Care Medicine 27.1 (2012): 11-24.

Bartynski, W. S. "Posterior reversible encephalopathy syndrome, part 1: fundamental imaging and clinical features." American Journal of Neuroradiology 29.6 (2008): 1036-1042.

Bartynski, W. S. "Posterior reversible encephalopathy syndrome, part 2: controversies surrounding pathophysiology of vasogenic edema." American Journal of Neuroradiology 29.6 (2008): 1043-1049.

Bradshaw, Michael J., and Arun Venkatesan. "Herpes simplex virus-1 encephalitis in adults: pathophysiology, diagnosis, and management.Neurotherapeutics 13.3 (2016): 493-508.

Sili, Uluhan, et al. "Herpes simplex virus encephalitis: clinical manifestations, diagnosis and outcome in 106 adult patients." Journal of Clinical Virology 60.2 (2014): 112-118.

Ellis, Colin A., et al. "Cerebrospinal fluid in posterior reversible encephalopathy syndrome: implications of elevated protein and pleocytosis." The Neurohospitalist 9.2 (2019): 58-64.