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LETTER TO EDITOR
Year : 2011  |  Volume : 59  |  Issue : 6  |  Page : 906-908

Diagnosing paroxysmal autonomic instability with dystonia following intracerebral hemorrhage


Department of Neurosurgery, LSU HSC in Shreveport, Shreveport, LA 71130, Louisiana, USA

Date of Submission10-Jul-2011
Date of Decision10-Jul-2011
Date of Acceptance14-Jul-2011
Date of Web Publication2-Jan-2012

Correspondence Address:
Bharat Guthikonda
Department of Neurosurgery, LSU HSC in Shreveport, Shreveport, LA 71130, Louisiana
USA
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DOI: 10.4103/0028-3886.91377

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How to cite this article:
Chittiboina P, Nixon M, Nanda A, Guthikonda B. Diagnosing paroxysmal autonomic instability with dystonia following intracerebral hemorrhage. Neurol India 2011;59:906-8

How to cite this URL:
Chittiboina P, Nixon M, Nanda A, Guthikonda B. Diagnosing paroxysmal autonomic instability with dystonia following intracerebral hemorrhage. Neurol India [serial online] 2011 [cited 2014 Sep 30];59:906-8. Available from: http://www.neurologyindia.com/text.asp?2011/59/6/906/91377


Sir,

Paroxysmal autonomic instability with dystonia (PAID) is seen in 8-33% of patients with severe brain injury. [1] The syndrome is characterized by agitation, diaphoresis, hyperthermia, tachycardia, hypertension, tachypnea, hypertonia, and extensor posturing. [2] To our knowledge, there are only three reported cases of PAID syndrome after intracerebral hemorrhage (ICH). [3],[4],[5] We present the fourth case of PAID in a patient with large ICH.

A 47-year-old African American female with a past medical history of uncontrolled hypertension was found down at work having witnessed seizure activity. Physical examination on arrival revealed a Glasgow Coma Score (GCS) of 12 (E4, V2, M6); pupils were round and briskly reactive with right hemiparesis. Computed tomography (CT) scan of head revealed a 4.0 cm × 4.4 cm left basal ganglia ICH with 8 mm shift [Figure 1]. Ten days later, her neurologic status deteriorated with bilateral extensor posturing. She was taken to the operating room for evacuation of ICH [Figure 2]. On postoperative day-11 she had an episode of agitation, tacyhpnea (44 bpm), tachycardia (122 bpm), increased BP (192/94), diaphoresis and extensor posturing with temperatures up to 38.3-39.5°C [Table 1]. Repeat CT head showed no acute pathology [Figure 3] and an electro-encephalogram (EEG) revealed no epileptiform activity. Upon transfer to neurosurgical floor on postoperative day-19, she had another dysautonomic episode. She was intubated and transferred back to the intensive care unit (ICU) with ventilator, cooling blanket, and benzodiazepines. She continued to have 2-3 episodes of autonomic instability per day. Beta-blockers and bromocriptine decreased her level of agitation and heart rate, with no change in other signs. A trial of IV morphine 5 mg was initiated during a "storming" episode resulting in resolution of PAID within 20 minutes. With adequate control of PAID, she was subsequently transferred to a long-term acute care facility for further management of her devastating neurological injury.
Figure 1: CT head without contrast at the time of admission revealing a 4.0 cm×4.4 cm left basal ganglia intracerebral hemorrhage with 8 mm midline shift. A ventriculostomy has been placed on the right side

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Figure 2: Postoperative CT head revealing a complete resection of ICH with an improvement in midline shift

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Figure 3: At the onset of PAID, a CT head revealed no new ICH or mass lesions. A hypodensity in the left basal ganglia was observed. Additionally, a sub-galeal collection was noted

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Table 1: The findings constituting PAID syndrome in the reported patient

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Currently, milder forms of autonomous instability are treated in the routine manner in ICUs with beta blockers and sedation. [6] Since the presence of PAID syndrome is associated with worse outcomes, recognition of this syndrome in patients with brain injury is important. [6],[7] With the knowledge that PAID may be a spectrum of diseases rather than one single entity, may lead to improved recognition and characterization. It has been speculated that PAID may lead to worse outcomes due to secondary brain injury from hyperthermia, increased ICP, or an extreme increase in energy expenditure. [6],[8] Early recognition may lead to fewer diagnostic tests and a rational approach to management. This is especially important as PAID can mimic other life-threatening conditions in the ICU. [2]

There are few reports of PAID following ICH [Table 2]. In patients with ICH, catecholamine/metanephrine peaks at twice normal range on day-7, analogous to PAID syndrome associated with TBI. The degree of dysautonomia is also proportional to the size of ICH. [9] The role of surgical evacuation in preventing this syndrome remains unknown. PAID may occur before [4] or after [3] evacuation of the ICH. The effect of ICH size on autonomic instability could be due to a global increase in ICP or through diencephalic disconnection. [7] In some cases, the location of the ICH could lead to diencephalic disconnection. On the other hand, non-diencephalic location like the frontal lobe has also been reported to lead to PAID. [3]
Table 2: Previous reports of PAID syndrome in patients with ICH

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Various pharmacological agents have been used for the management of PAID syndrome. The drugs most commonly include beta blockers like propranolol, opiate agonist like morphine, GABA B agonist like baclofen or dopamine agonist like bromocriptine. [1] With the demonstration of successful abruption of a full blown PAID morphine, we were able to transfer the patient from ICU to the neurosurgical floor. An appropriate recognition and treatment of PAID syndrome resulted in an improved management of the signs on a regular neurosurgical floor.

 
  References Top

1.Baguley IJ. Autonomic complications following central nervous system injury. Semin Neurol 2008;28:716-25.  Back to cited text no. 1
[PUBMED]  [FULLTEXT]  
2.Blackman JA, Patrick PD, Buck ML, Rust RS Jr. Paroxysmal autonomic instability with dystonia after brain injury. Arch Neurol 2004;61:321-8.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.Becker R, Benes L, Sure U, Hellwig D, Bertalanffy H. Intrathecal baclofen alleviates autonomic dysfunction in severe brain injury. J Clin Neurosci 2000;7:316-9.  Back to cited text no. 3
[PUBMED]  [FULLTEXT]  
4.Rossitch E Jr, Bullard DE. The autonomic dysfunction syndrome: Aetiology and treatment. Br J Neurosurg 1988;2:471-8.  Back to cited text no. 4
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5.Tong C, König MW, Roberts PR, Tatter SB, Li XH. Autonomic dysfunction secondary to intracere-bral hemorrhage. Anesth Analg 2000;91:1450-1.  Back to cited text no. 5
    
6.Rabinstein AA. Paroxysmal autonomic instability after brain injury. Arch Neurol 2004;61:1625.  Back to cited text no. 6
[PUBMED]  [FULLTEXT]  
7.Baguley IJ, Nott MT, Slewa-Younan S, Heriseanu RE, Perkes IE. Diagnosing dysautonomia after acute traumatic brain injury: Evidence for overresponsiveness to afferent stimuli. Arch Phys Med Rehabil 2009;90:580-6.  Back to cited text no. 7
[PUBMED]  [FULLTEXT]  
8.Leow MK, Loh KC, Kiat Kwek T, Ng PY. Catecholamine and metanephrine excess in intracerebral haemorrhage: Revisiting an obscure yet common "pseudophaeochromocytoma." J Clin Pathol 2007;60:583-4.  Back to cited text no. 8
[PUBMED]  [FULLTEXT]  
9.Diamond AL, Callison RC, Shokri J, Cruz-Flores S, Kinsella LJ. Paroxysmal sympathetic storm. Neurocrit Care 2005;2:288-91.  Back to cited text no. 9
[PUBMED]  [FULLTEXT]  


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