Limits...
Posterior reversible encephalopathy syndrome in a patient with a Chiari I malformation.

Hansberry DR, Agarwal N, Tomei KL, Goldstein IM - Surg Neurol Int (2013)

Bottom Line: Further workup showed evidence of PRES.After weaning pressors, the patient had a significant progressive improvement in her mental status.Although the mechanism of PRES remains controversial given its diverse clinical presentation, several theories implicate hypertension and steroid use as causative agents.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurological Surgery, Rutgers New Jersey Medical School, Newark, New Jersey, USA.

ABSTRACT

Background: The authors describe a unique case of a patient who developed posterior reversible encephalopathy syndrome (PRES) following postoperative treatment of a Chiari I malformation.

Case decsription: A 25-year-old female presented with complaints of left upper and lower extremity paresthesias and gait disturbances. A magnetic resonance imaging (MRI) of the brain and cervical spine showed a Chiari I malformation with tonsillar descent beyond the level of the C1 lamina. She underwent a suboccipital craniectomy and C1 laminectomy with cerebellar tonsillar cauterization and duraplasty. Postoperatively, an MRI showed bilateral acute infarcts of the cerebellar vermis. She was initially treated for cerebellar ischemia with hypertensive therapy with a subsequent decline in her neurologic status and generalized tonic-clonic seizure. Further workup showed evidence of PRES. After weaning pressors, the patient had a significant progressive improvement in her mental status.

Conclusion: Although the mechanism of PRES remains controversial given its diverse clinical presentation, several theories implicate hypertension and steroid use as causative agents.

No MeSH data available.


Related in: MedlinePlus

Diffusion Weighted Imaging (DWI) (a) and T2 axial FLAIR MRI (b) on postoperative day 9 showing increased signal in the bilateral frontal and parietal lobes, consistent with PRES
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3814995&req=5

Figure 4: Diffusion Weighted Imaging (DWI) (a) and T2 axial FLAIR MRI (b) on postoperative day 9 showing increased signal in the bilateral frontal and parietal lobes, consistent with PRES

Mentions: She was readmitted to the hospital from rehab 6 days after discharge with complaints of worsening of her swallowing. She also noted left sided pain and worsening weakness. At this point her exam had declined from her postoperative exam and motor exam now revealed 3/5 strength in left dorsiflexion and extensor hallucis longus. At the time of readmission, she was normotensive with a blood pressure of 130/70. A swallow evaluation revealed significant aspiration. She underwent an MRI that showed bilateral acute infarcts of the cerebellar vermis [Figure 3]. We did not have a clear explanation for this increase from her postoperative scan. Given the evolution of the infarct she was started on pressors to increase her systolic parameters to 160-180 mmHg and optimize perfusion in the setting of ischemia. Two days after initiating pressors, the patient had a generalized tonic–clonic seizure. A CT of the head at that time demonstrated diffuse loss of sulci with effacement of the suprasellar and quadrigeminal cisterns. She was subsequently intubated for worsening mental status and lethargy. A follow-up MRI revealed diffuse bifrontal and parietal gray matter hyperintensity on FLAIR without changes on diffusion-weighted imaging consistent with PRES and suggestive of edema from hypoxic ischemic changes secondary to prior seizure [Figure 4]. An electroencephalography (EEG) showed no further seizure activity and CSF cultures were negative. She underwent an angiogram to evaluate for vasospasm as a possible etiology of her evolving infarcts, which showed no evidence of vasospasm or vasculitis. Following those results, the pressors were weaned off. A repeat CT of the head was obtained, which showed increasing cerebral edema. As a result of the increasing edema and her compromised neurologic exam, an intracranial pressure (ICP) monitor was placed and maintained for 2 days, which showed low opening pressure, and ICPs ranging from 1 to 7. Follow-up MRIs demonstrated progressive resolution of the cerebral edema and FLAIR signal [Figure 5] with complete resolution at 2 years postoperative [Figure 6].


Posterior reversible encephalopathy syndrome in a patient with a Chiari I malformation.

Hansberry DR, Agarwal N, Tomei KL, Goldstein IM - Surg Neurol Int (2013)

Diffusion Weighted Imaging (DWI) (a) and T2 axial FLAIR MRI (b) on postoperative day 9 showing increased signal in the bilateral frontal and parietal lobes, consistent with PRES
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3814995&req=5

Figure 4: Diffusion Weighted Imaging (DWI) (a) and T2 axial FLAIR MRI (b) on postoperative day 9 showing increased signal in the bilateral frontal and parietal lobes, consistent with PRES
Mentions: She was readmitted to the hospital from rehab 6 days after discharge with complaints of worsening of her swallowing. She also noted left sided pain and worsening weakness. At this point her exam had declined from her postoperative exam and motor exam now revealed 3/5 strength in left dorsiflexion and extensor hallucis longus. At the time of readmission, she was normotensive with a blood pressure of 130/70. A swallow evaluation revealed significant aspiration. She underwent an MRI that showed bilateral acute infarcts of the cerebellar vermis [Figure 3]. We did not have a clear explanation for this increase from her postoperative scan. Given the evolution of the infarct she was started on pressors to increase her systolic parameters to 160-180 mmHg and optimize perfusion in the setting of ischemia. Two days after initiating pressors, the patient had a generalized tonic–clonic seizure. A CT of the head at that time demonstrated diffuse loss of sulci with effacement of the suprasellar and quadrigeminal cisterns. She was subsequently intubated for worsening mental status and lethargy. A follow-up MRI revealed diffuse bifrontal and parietal gray matter hyperintensity on FLAIR without changes on diffusion-weighted imaging consistent with PRES and suggestive of edema from hypoxic ischemic changes secondary to prior seizure [Figure 4]. An electroencephalography (EEG) showed no further seizure activity and CSF cultures were negative. She underwent an angiogram to evaluate for vasospasm as a possible etiology of her evolving infarcts, which showed no evidence of vasospasm or vasculitis. Following those results, the pressors were weaned off. A repeat CT of the head was obtained, which showed increasing cerebral edema. As a result of the increasing edema and her compromised neurologic exam, an intracranial pressure (ICP) monitor was placed and maintained for 2 days, which showed low opening pressure, and ICPs ranging from 1 to 7. Follow-up MRIs demonstrated progressive resolution of the cerebral edema and FLAIR signal [Figure 5] with complete resolution at 2 years postoperative [Figure 6].

Bottom Line: Further workup showed evidence of PRES.After weaning pressors, the patient had a significant progressive improvement in her mental status.Although the mechanism of PRES remains controversial given its diverse clinical presentation, several theories implicate hypertension and steroid use as causative agents.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurological Surgery, Rutgers New Jersey Medical School, Newark, New Jersey, USA.

ABSTRACT

Background: The authors describe a unique case of a patient who developed posterior reversible encephalopathy syndrome (PRES) following postoperative treatment of a Chiari I malformation.

Case decsription: A 25-year-old female presented with complaints of left upper and lower extremity paresthesias and gait disturbances. A magnetic resonance imaging (MRI) of the brain and cervical spine showed a Chiari I malformation with tonsillar descent beyond the level of the C1 lamina. She underwent a suboccipital craniectomy and C1 laminectomy with cerebellar tonsillar cauterization and duraplasty. Postoperatively, an MRI showed bilateral acute infarcts of the cerebellar vermis. She was initially treated for cerebellar ischemia with hypertensive therapy with a subsequent decline in her neurologic status and generalized tonic-clonic seizure. Further workup showed evidence of PRES. After weaning pressors, the patient had a significant progressive improvement in her mental status.

Conclusion: Although the mechanism of PRES remains controversial given its diverse clinical presentation, several theories implicate hypertension and steroid use as causative agents.

No MeSH data available.


Related in: MedlinePlus