Can neurostorming occur without diffuse axonal injury?

Neurostorming Can Occur Without Diffuse Axonal Injury

Yes, neurostorming (paroxysmal sympathetic hyperactivity) can occur without diffuse axonal injury, as it can develop in various types of brain injuries beyond DAI, including focal injuries, hypoxic-ischemic injuries, and other forms of traumatic brain injury.

Understanding Neurostorming and Its Relationship to Brain Injury

Neurostorming, also known as paroxysmal sympathetic hyperactivity (PSH), is characterized by episodes of:

• Tachycardia, hypertension, tachypnea, hyperthermia, diaphoresis, and posturing 1
• Symptoms typically occurring in a paroxysmal pattern with periods of relative normalcy between episodes 2
• Episodes that can be triggered by external stimuli such as repositioning, suctioning, or other care activities 1

Brain Injury Patterns Associated with Neurostorming

Diffuse Axonal Injury

• DAI is present in approximately 50% of cases with severe traumatic brain injury 3
• Classified into three grades based on location of axonal lesions:
  • Grade I: Axonal lesions in cerebral hemispheres
  • Grade II: Focal axonal lesions in corpus callosum
  • Grade III: Focal or multiple axonal lesions in brainstem 3, 4
• DAI commonly causes neurostorming, especially with brainstem involvement 1

Other Brain Injury Patterns Associated with Neurostorming

• Hypoxic-ischemic brain injury can trigger neurostorming without DAI being present 5
• Symptomatic hypoxic-ischemic injury with diffuse brain cell death can present with global neurological signs 5
• Focal traumatic lesions affecting autonomic centers or pathways can cause neurostorming 2
• Cerebral contusions without DAI can lead to neurostorming 1, 2

Evidence Supporting Neurostorming Without DAI

• Hypoxic-ischemic brain injury can cause diffuse brain, spinal cord, or retinal cell death attributable to hypotension or hypoxia without axonal injury 5
• Neurostorming has been documented in cases of anoxic brain injury where the primary mechanism is not axonal shearing 5
• Cases have been reported where patients developed delayed onset of coma and neurological symptoms consistent with neurostorming even without direct head trauma 6

Diagnostic Considerations

• Non-contrast CT is the first-line imaging modality in acute TBI but has limitations in detecting both DAI and early signs of neurostorming 1
• MRI is indicated when CT results are normal but persistent unexplained neurologic findings are present 1, 2
• Specific MRI sequences for optimal detection:
  • T2*-weighted gradient-echo imaging for microhemorrhages
  • Susceptibility-weighted imaging (SWI) - 3-6 times more sensitive than T2* GRE
  • Diffusion-weighted imaging (DWI) for non-hemorrhagic axonal injuries 1

Management Implications

• Management of neurostorming focuses on symptom control regardless of underlying etiology 2
• Treatment strategies include:
  • Maintaining adequate cerebral perfusion with systolic BP >110 mmHg 2
  • Controlling ventilation through intubation and mechanical ventilation when necessary 2
  • Preventing secondary brain injury through avoidance of hypocapnia 2
  • Early physical therapy to prevent contractures 2

Clinical Pearls and Pitfalls

• Neurostorming is often underdiagnosed or misdiagnosed as seizures, agitation, or pain 2
• The absence of DAI on imaging does not rule out the possibility of neurostorming 1
• Regular neurological assessments are crucial to detect clinical deterioration in all types of brain injury 2
• Multidisciplinary case reviews are recommended for patients with severe symptoms regardless of underlying pathology 1, 2