Published 2 September 2009, doi:10.1136/bmj.b3343
Cite this as: BMJ 2009;339:b3343

Endgames

Picture quiz

Stroke quiz

Asif Atik Mazumder, registrar, geriatric medicine1, George Anthony Pope, clinical fellow, stroke medicine1

1 Department of Stroke Medicine, King’s College Hospital, London SE1 6AW

Correspondence to: A A Mazumder asifmaz{at}gmail.com

A 77 year old right handed man presented after a collapse. He was found to have a dense right sided hemiplegia, with the right arm worse than the right leg and "forehead sparing" facial weakness. He was aphasic, with his gaze preference to the left. His symptoms had been present for 30 minutes and did not improve. No signs of meningism were present. Computed tomography of the head was performed immediately (fig 1Go) and 24 hours after thrombolytic treatment (fig 2Go).


Figure 1
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Fig 1 Computed tomogram of the head at presentation

 


Figure 2
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Fig 2 Computed tomogram of the head 24 hours after thrombolytic treatment

 

Questions

1 What feature is seen in fig 1?
2 What other stroke signs could be expected on examination?
3 What complication of treatment is evident in fig 2?
4 Using the assessment scale developed by the European Cooperative Acute Stroke Study (ECASS), which category does the scan in fig 2 fit into?

Answers

Short answers

1 Middle cerebral artery dot sign.
2 Eye deviation towards the side of the infarction; contralateral hemianopia; contralateral sensory loss; global aphasia; apraxia; and visual, motor, and sensory neglect.
3 Post-thrombolysis multifocal intraparenchymal haematomas with a midline shift.
4 Parenchymatous haemorrhage category 2 (PH2)—blood in more than 30% of the infarct area, with a substantial space effect.

Long answers
1 Feature on computed tomography
The computed tomography scan performed immediately after presentation (fig 3Go) shows an area of hyperdensity in the distal middle cerebral artery seen in the sylvian fissure on the left. The middle cerebral artery dot sign is an early marker of thromboembolic occlusion of distal middle cerebral artery branches seen in the sylvian fissure.1


Figure 3
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Fig 3 Non-contrast enhanced computed tomography scan of the patient’s head showing an area of hyperdensity in the distal middle cerebral artery seen in the sylvian fissure on the left (arrow)

 
It is important to recognise early signs of stroke given the advent of thrombolysis and the need to deliver recombinant tissue plasminogen activator within three hours. Other more subtle signs of early infarction exist, and can be discreetly assessed using the ASPECT (Alberta stroke program early computed tomography) score.2 3 Such scoring systems allow more robust assessment of computed tomography scans for stroke and reduce interobserver variability.

2 Other signs
This patient is right handed, so his left hemisphere is dominant. Symptoms of middle cerebral artery stroke include contralateral hemiplegia, gaze deviation towards the side of the stroke, contralateral hemianopia, and contralateral hemisensory loss. It is important to note, however, that hemisensory neglect and visuospatial impairments are uncommon in left sided infarcts.

Signs of dominant hemisphere middle cerebral artery stroke include:

Global aphasia (Broca’s aphasia, Wernicke’s aphasia, and conductive aphasia)
Apraxias (usually ideomotor apraxia and ideational apraxia)
Gerstmann’s syndrome:4
  • Agraphia
  • Dyscalculia
  • Right-left disorientation
  • Finger agnosia.

Sixty per cent of left handed people also have a left sided dominant hemisphere. Signs of non-dominant hemisphere stroke are more difficult to elicit and are often overlooked.5 These include:

Dysarthria
Hemineglect
Constructional and dressing apraxias
Topographical agnosia
Astereognosis (inability to recognise objects placed in the hand)
Anosognosia (inability to recognise a deficit)
Aprosody (inability to vary intonation of speech)
Affective agnosia.

3 Complication of treatment
The computed tomography scan performed 24 hours after treatment shows two areas of haematoma within the left cerebral hemisphere (fig 4Go). Of note also is the effacement of the cerebral sulci, compression of the posterior horn of the left lateral ventricle, and a 4 mm midline shift to the right.


Figure 4
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Fig 4 Computed tomography scan of the patient’s head 24 hours after treatment showing two areas of haematoma within the left cerebral hemisphere (arrows)

 
After thrombolysis patients should be admitted to an acute stroke unit, where they can be monitored closely for neurological deterioration suggestive of intracerebral bleeding. The National Institute of Neurological Disorders and Stroke study found that symptomatic haemorrhage within 36 hours of stroke occurred in 6.4% of patients treated with tissue plasminogen activator compared with 0.6% of the placebo group.6 Intracerebral haemorrage that occurs more than 36 hours after treatment is not thought to be related to tissue plasminogen activator.6 7 Urgent discussion with the neurosurgical team would be warranted. It has been recognised recently that the management of post-thrombolysis haemorrhage is complex.8 It is important to assess the patient using the National Institute of Health Stroke Scale (NIHSS) before treatment. The NIHSS score is an objective clinical measurement of the severity of acute ischaemic stroke. A high NIHSS score (indicative of a severe stroke) is an independent risk factor for intracerebral haemorrhage after treatment with tissue plasminogen activator.9 10 The National Institute of Neurological Disorders and Stroke study found that an NIHSS score greater than 20 was associated with an 11-fold increased risk of symptomatic intracerebral haemorrhage compared with a score of 5 or less after thrombolytic treatment.6 However, the NIHSS score should be considered in combination with other factors that influence the risk to benefit ratio of thrombolytic treatment after stroke, including brain oedema and mass effect.6 Strict management of blood pressure to a therapeutic protocol is also suggested, as well as careful attention to pretherapeutic glycaemic values.11

4 ECASS category
The grading system pioneered by the European Cooperative Acute Stroke study categorises haemorrhagic transformation of strokes after thrombolysis into the following groups12 13:

H0: no haemorrhage detected
HI1: haemorrhagic infarct category 1—small petechiae along the periphery of the infarct
HI2: haemorrhagic infarct category 2—confluent petechiae within infarct area, but no space effect
PH1: parenchymatous haemorrhage category 1—blood in less than 30% of the infarct area, may have a slight space effect
PH2: parenchymatous haemorrhage category 2—blood in more than 30% of the infarct area, substantial space effect.

Patient outcome
The patient was discharged after comprehensive multidisciplinary input on the stroke unit. At home, he needed help with dressing, washing, and climbing stairs.

Cite this as: BMJ 2009;339:b3343


Competing interests: None declared.

Provenance and peer review: Not commissioned; externally peer reviewed.

Patient consent obtained.

References

  1. Barber PA, Demchuk AM, Hudon ME, Pexman JH, Hill MD, Buchan AM. Hyperdense sylvian fissure MCA "dot" sign: a CT marker of acute ischemia. Stroke 2001;32:84-8.[Abstract/Free Full Text]
  2. Tomsick T, Brott T, Barsan W, Broderick J, Haley EC, Spilker J, et al. Prognostic value of the hyperdense middle cerebral artery sign and stroke scale score before ultraearly thrombolytic therapy. AJNR Am J Neuroradiol 1996;17:79-85.[Abstract]
  3. Pexman JH, Barber PA, Hill MD, Sevick RJ, Demchuk AM, Hudon ME, et al. Use of the Alberta stroke program early CT score (ASPECTS) for assessing CT scans in patients with acute stroke. AJNR Am J Neuroradiol 2001;22:1534-42.[Abstract/Free Full Text]
  4. Gerstmann J, The syndrome of finger agnosia, disorientation for right and left, agraphia and acalculia. J Neurol Neurosurg Psychiatry 1940;44:398-408.
  5. Di Legge S, Fang J, Saposnik G, Hachinski V. The impact of lesion side on acute stroke treatment. Neurology 2005;65:81-6.[Abstract/Free Full Text]
  6. National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Intracerebral hemorrhage after intravenous t-PA therapy for ischemic stroke. Stroke 1997;28:2109-18.[Abstract/Free Full Text]
  7. Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. N Engl J Med 1995;333:1581-7.[Abstract/Free Full Text]
  8. Derex L, Nighoghossian N. Intracerebral haemorrhage after thrombolysis for acute ischemic stroke: an update. J Neurol Neurosurg Psychiatry 2008;79:1093-9.[Abstract/Free Full Text]
  9. Larrue V, von Kummer R, del Zoppo G, Bluhmki E. Hemorrhagic transformation in acute ischaemic stroke: potential contributing factors in the European Cooperative Acute Stroke Study. Stroke 1997;28:957-60.[Abstract/Free Full Text]
  10. Tanne D, Kasner SE, Demchuk AM, Koren-Morag N, Hanson S, Grond M, et al. Markers of increased risk of intracerebral hemorrhage after intravenous recombinant tissue plasminogen activator therapy for acute ischaemic stroke in clinical practice: Multicentre rt-PA Stroke Survey. Circulation 2002;105:1679-85.[Abstract/Free Full Text]
  11. Demchuk AM, Morgenstern LB, Krieger DW, Linda Chi T, Hu W, Wein TH, et al. Serum glucose level and diabetes predict tissue plasminogen activator-related intracerebral hemorrhage in acute ischemic stroke. Stroke 1999;30:34-9.[Abstract/Free Full Text]
  12. Hacke W, Kaste M, Fieschi C, Toni D, Lesaffre E, von Kummer R, et al. Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke: the European Cooperative Acute Stroke Study (ECASS). JAMA 1995;274:1017-25.[Abstract/Free Full Text]
  13. Hacke W, Kaste M, Fieschi C, von Kummer R, Davalos A, Meier D, et al. Randomised double-blind placebo-controlled trial of thrombolytic therapy with intravenous alteplase in acute ischaemic stroke (ECASS II). Lancet 1998;352:1245-51.[CrossRef][Web of Science][Medline]

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