A 34-Year-Old Woman With Headache, Dizziness, And Poor Coordination

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Background

A 34-year-old woman presents to the emergency department (ED) with a 3-day history of pain around the right ear extending

the temple. She was sitting at work today when she suddenly experienced dizziness, a feeling of discomfort in the throat, and

burning sensation in the left arm and leg. When she tried to stand and walk, her right arm and leg did not move in a normal,

coordinated manner. The patient was previously healthy and does not take any regular medications. She does not smoke or

drink. She does vigorous aerobic exercises on an almost daily basis. Her mother and a number of relatives on her mother's

side suffer from hypertension.

On physical examination, the patient has an oral temperature of 98.6F (37.0C). Her pulse is regular with a rate of 86 bpm.

Her blood pressure is 164/90 mm Hg, and her heart sounds are normal and without added sounds. There are no arterial brui

auscultated in her neck. She is noted to have prolonged bouts ofhiccuping. She is unable to stand due to a severe feeling of

imbalance. There is right-sided ptosis and miosis. She has a sustained horizontal gaze-evoked nystagmus looking to the leftand right, with a downbeating nystagmus on downward gaze. There is decreased sensation of pinprick and temperature on t

right side of the face. On the right side there is also reduced movement of the palate, and the gag reflex is diminished. The

tongue movements are normal. The power is normal in all 4 limbs, the deep tendon reflexes are normal, and the plantar

responses are downgoing bilaterally (there is no Babinski sign). There is a moderate degree of ataxia affecting the right arm

and leg. There is decreased sensation to pinprick and temperature on the left arm, leg, and trunk. The joint position and

vibration sense are intact bilaterally.

Routine laboratory analysis, including a complete blood cell count, a basic metabolic panel, and a lipid profile, is normal. A

noncontrast computed tomography (CT) scan of the head is normal. Magnetic resonance imaging (MRI) of the brain is obtain

(Figure 1).

What is the diagnosis?

Hint: Consider the cranial nerves involved, and which sensory modalities are affected.

Right-sided lateral pontine stroke (ie. Marie-Foix syndrome)

Right-sided lateral medullary stroke (ie, Wallenberg syndrome)

Right-sided medial medullary stroke (ie, Dejerine syndrome)

Right-sided hemi-medullary stroke (ie, Babinski-Nageotte syndrome)

Left-sided medial medullary stroke

Save and Proceed

Would you like to see other radiologic images of vessel occlusion? Click here to see more:

A 34-Year-Old Woman With Headache, Dizziness, and PoorCoordination

Ajith Goonetilleke, MB BS, FRCP

Posted: 10/29/2010


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Imaging Findings of Vessel Occlusion: Slideshow

Discussion

The patient in this case was diagnosed with a lateral medullary stroke on the right with Wallenberg syndrome.

Neurons relaying pain and temperature sensation from the right side of the face synapse in the descending spinal nucleus of

Figure 1.


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the trigeminal nerve, which lies in the dorsolateral aspect of the brainstem (Figure 2). Thereafter, the pathway crosses (as the

quintothalamic tracts) and ascends to the thalamus. For the limbs and trunk, the neurons of the spinothalamic tract from the

side of the body pass into the spinal cord, where they ascend for 1 or 2 levels (via Lissauer's tract) and then synapse. The

second-order neurons then cross to the right side of the spinal cord (via the anterior commissure, just anterior to the central

canal of the cord) and then ascend in the anterolateral aspect of the spinal cord up into the right side of the brainstem. In the

brainstem, the spinothalamic tract lies laterally.

Figure 1.


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This patient had impairment of pain and temperature (ie, spinothalamic) sensation on the right side of the face and the left sid

of the body. These contralateral findings are characteristic of a right lateral medullary lesion. The patient also had reduced

palatal movements and gag reflex on the right side indicative of involvement of the right IX (glossopharyngeal) and X (vagus)

cranial nerves. These cranial nerves, as well as the descending sympathetic fibers (patient had a right-sided Horner sign), ar

also found in the dorsolateral aspect of the right side of the medulla (Figure 2). The presence ofvertigo and right-sided ataxia

Figure 1.


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was due to involvement of the vestibular nucleus and cerebellar pathways (as they pass into the cerebellum through the infe

cerebellar peduncle), respectively, on the right side. The nucleus and the fascicles of the hypoglossal nerve lie medially withi

the medulla, and the pyramidal pathways lie anteromedially as they pass through the medulla. The joint position and vibratio

sense modalities pass up the spinal cord on the ipsilateral side and then synapse at the gracile and cuneate nuclei in the low

part of the medulla. The dorsal column pathways then cross (as the internal arcuate fibres) at the level of the lower medulla a

pass up the medial aspect of the brainstem as the medial lemnisci. The normal tongue movements and the preserved

pyramidal and dorsal column function in this patient indicated that there was sparing of the medial medulla; therefore, this

patient had a right-sided lateral medullary syndrome (ie, Wallenberg syndrome), which was determined by brain MRI to be a

stroke. The T2-weighted coronal scan showed a high signal abnormality in the right side of the medulla (black arrow, Figure

The presence of prominent right ear pain for 3 days prior to developing neurologic deficits was suggestive of a vertebral arterdissection. In fact, stroke preceded by headache or neck pain should always raise suspicion for cervical arterial dissection. T

patient performed vigorous aerobic exercises on an almost daily basis, and these exercises included repetitive high-energy

lateral neck flexions. This is likely to have been the cause of an arterial dissection. The diagnosis made was of a dissection o

the right vertebral artery and a subsequent infarction of the dorsolateral aspect of the right medulla.

The lateral medullary syndrome (also called Wallenberg orposterior inferior cerebellar artery [PICA] syndrome) was first

described by Gaspard Vieusseux in 1808. Subsequent clinical (1895) and autopsy (1901) descriptions by Wallenberg led to t

syndrome being associated with his name. The loss of pain and temperature sensation on the ipsilateral side of the face and

Figure 2.


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contralateral side of the body is characteristic of this condition. Other clinical features include intractable hiccups, vertigo,

Horner syndrome,

nystagmus, dysarthria,

dysphagia, and ipsilatera

ataxia. The blood supply

the medulla is mainly fro

the vertebral arteries. At

the level of the lower

medulla, each vertebral

artery gives off a variable

branch named the poste

inferior cerebellar artery

(which may be absent in

to 25% of the population

that supplies the

dorsolateral aspects of th

medulla. At a higher leve

approaching the

pontomedullary junction,

each vertebral artery als

contributes branches to

form the anterior spinal

artery, which descends

over the anterior surface

the medulla and supplies

the medial aspects of the

medulla. The majority of

cases of Wallenberg

syndrome are therefore

due to vascular events,

whereby the dorsolatera

aspect of the medulla ma

be involved, with sparing

the medial medulla due to an intact anterior spinal artery supply. Definitive pathologic[1] and more recent MRI[2] studies indic

that lateral medullary infarctions occur due to involvement of the vertebral artery in 38% of cases. PICA is involved 14%-24%

the time, and both arteries are involved in 26% of cases. No abnormality is found in either vessel only 12%-19% of the time.

Intravenous thrombolysis (IVT) is an acute treatment of the lateral medullary syndrome. Although still very controversial, som

studies show that IVT using recombinant tissue plasminogen activator (tPA) is efficacious for acute ischemic stroke.[3]

Dissection is not an absolute contraindication to IVT; however, if a vertebral artery dissection extends intracranially (which is

uncommon), caution is advised due to an increased risk for bleeding. The ECASS 3 trial recently demonstrated benefit of IVT

given up to 4.5 hours after symptom onset in ischemic stroke, although certain patients were excluded from this trial and this

practice is not standard of care.[4] Newer, invasive, stent-based techniques exist for stroke and dissection treatment, though

they are available at very few centers. If a patient with a nonhemorrhagic stroke is seen beyond the time window for IVT, the

aspirin may be given. In this case, because there was a vertebral artery dissection, anticoagulation with heparin and

subsequently warfarin was indicated.

The mechanism of the intractable hiccups that is often observed in the lateral medullary syndrome is poorly understood.

Occasionally, gabapentin or chlorpromazine is effective. Patients may experience disturbed vision due to persistent nystagm

Figure 3.


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and this may be helped by gabapentin or memantine.[5]

Cervical artery dissections (CADs) may involve the carotid or vertebral arteries. They are implicated in 2% of all ischemic

strokes but in up to 10%-25% of cases in young and middle-aged patients. CAD may occur spontaneously, and several

inheritable connective tissue disorders (eg, Ehlers-Danlos syndrome type IV, Marfan syndrome, autosomal dominant polycys

Figure 1.


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kidney disease, and osteogenesis imperfecta) are associated with an increased risk. Familial arterial dissections have been

associated with generalized lentiginosis, coarctation of the aorta, bicuspid aortic valve, and aortic root dilatation. Traumatic

CAD occurs most frequently following motor vehicle accidents. Less violent forms oftrauma have also been implicated in CA

especially cervical spine chiropractic manipulations. Other forms oftrauma implicated in CAD include contact sports, yoga,

calisthenics, vigorous aerobic exercise, ceiling painting, tonic-clonic seizures, and riding on roller coasters. The mechanism o

stroke in CAD is usually thromboembolic due to disruption of normal blood flow in the region of dissection. Less commonly,

there may be partial or total occlusion of the vessel, which then results in low blood flow and watershed ischemia. The

presence of a CAD may be confirmed by formal cerebral angiography, but less invasive procedures such as MR angiography

CT angiography, or duplex Doppler studies are diagnostic in a high proportion of patients.

The patient in this case presented acutely to the ED, had a normal CT head scan, and was within the time window to receive

treatment with IVT. She was given 0.9 mg/kg of recombinant tPA intravenously 3 hours and 15 minutes after the onset of herstroke. She remained well, and 24 hours later she was started on oral aspirin therapy. Her intractable hiccups were treated w

oral chlorpromazine and resolved after 2 weeks. Because she was experiencing an intrusive burning sensation affecting the

side of her body as well as disturbed vision due to persistent nystagmus, she was started on gabapentin therapy. Both of the

symptoms were controlled well with gabapentin at 1800 mg per day. The patient's dysphagia and right-sided limb ataxia

improved such that she was able to eat a normal diet and walk within 1 week of hospital admission. The patient was

discharged to home and was able to return to her employment as an accountant 10 weeks after herstroke.

Physicians only: would you like to discuss this case study with other physicians? Visit Medscape Physician Connect to post

Figure 2.


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your thoughts and view comments from your colleagues.

You are seeing a

patient in whom you

suspect a brainstem

stroke due to avertebral artery

dissection. Which of

the following

investigations is

most appropriate

after an initial

noncontrast CT scan

of the head?

Echocardiography

Genetic testing for

Marfan syndrome

MRI head scan

and MR angiography

Lumbar puncture

The patient

described above is

found to have a

vertebral artery

dissection and stroke

with Wallenbergsyndrome. Which

symptom or sign

would you expect to

find in this patient?

Hemiplegia

Contralateral ataxia

Ipsilateral decreased temperature sensation on the face

Contralateral decreased pinprick sensation on the face

Save and Proceed

Would you like to see other radiologic images of vessel occlusion? Click here to see more:

Imaging Findings of Vessel Occlusion: Slideshow

Figure 3.


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Medscape 2010 WebMD, LLC

References

1. Fisher CM, Karnes WE, Kubik CS. Lateral medullary infarction: the pattern of vascular occlusion. J Neuropathol Exp

Neurol. 1961;20:323-379. [MEDLINE: 13699936]

2. Kim JS, Lee JH, Choi CG. Patterns of lateral medullary infarction: vascular lesion-magnetic resonance imaging

correlation of 34 cases. Stroke. 1998;29:645-652. [MEDLINE: 9506607]

3. 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;333:1581-1587. [MEDLINE: 7477192]

4. Hacke W, Kaste M, Bluhmki E, et al; ECASS Investigators. Thrombolysis with alteplase 3 to 4.5 hours after acute

ischemic stroke. N Engl J Med. 2008;359:1317-1329. [MEDLINE: 18815396]

5. Thurtell MJ, Joshi AC, Leone AC, et al. Crossover trial of gabapentin and memantine as treatment for acquired

nystagmus. Ann Neurol. 2010;67:676-680. [MEDLINE: 20437565]

6. Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early management of adults with ischemic stroke: a

guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Coun

Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality

Care Outcomes in Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the value

this guideline as an educational tool for neurologists. Stroke. 2007;38:1655-1711. [MEDLINE: 17431204]

7. Engelter ST, Rutgers MP, Hatz F, et al. Intravenous thrombolysis in stroke attributable to cervical artery dissection.

Stroke. 2009;40:3772-3776. [MEDLINE: 19834022]

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