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Neuroprotection (Acute Phase)


Nimodipine is a calcium channel blocker initially developed to treat high BP. Its mechanism of action in treating acute SCI is thought to include lowering of BP and slowing the flow of calcium into blood vessels to reduce injury related ischemia (Fehlings & Baptiste 2005). Nimodipine has only been investigated in one clinical trial for acute SCI in humans to date.

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Pointillart et al. (2000) (English translation of Petitjean et al. (1998))





Population: Age range=20-47 yr; Gender: male=90%, female=10%; Level of injury: not specified; Severity of injury: complete=45%, incomplete=55%.

Treatment: Patients were randomly assigned to one of four groups: methylprednisolone (MP), nimodipine, MP + nimodipine, or no treatment. The dosages of nimodipine were 0.15 mg/kg/h over 2 hr followed by 0.03 mg/kg/h for 7 days. The dosages of MP followed National Acute Spinal Cord Injury Study (NASCIS) II guidelines and were 30 mg/kg over 1 hr followed by 5.4 mg/kg/h for 23 hr.

Outcome Measures: The following after 1 year: neurological function based on American Spinal Injury Association (ASIA) score (motor and sensory), adverse event outcomes.

Chronicity: Individuals were hospitalized within 8 hr of sustaining injury.

  1. After 1 year, there were no significant differences in neurological recovery based on ASIA scores among the four groups (p>0.05).
  2. Patients who received nimodipine and those who received no medication had significantly lower rates of hyperglycemia than patients who received MP (p<0.05).
  3. The authors noted that patients with incomplete injuries experienced significantly more neurological recovery than patients with complete injuries (p<0.0001).


Pointillart et al. (2000) did not find any significant differences in terms of neurological recovery among individuals receiving MP, nimodipine, MP plus nimodipine, or no treatment.Animal studies have shown that nimodipine on its own may not be beneficial for treating SCI (Faden et al. 1984aFord & Malm 1985), but when used in combination with other agents, such as adrenaline, there were significant effects on enhancing spinal cord blood flow (Ross & Tator 1991). Larger, randomized clinical trials are necessary to determine the effectiveness of nimodipine on neurological recovery in acute SCI.


There is level 1b evidence (from one RCT: Pointillart et al. 2000) that nimodipine is not effective in promoting neurological recovery in acute SCI individuals.

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