A 67-year-old woman comes to the office for follow-up. Four weeks ago, she experienced sudden-onset numbness on the right side, and evaluation revealed an ischemic stroke. The patient feels as if some of her sensation is returning but experiences transient burning pain in the right upper and lower limbs that can be induced even by a light touch. Medical history is significant for hypertension and type 2 diabetes mellitus. The patient smoked half a pack of cigarettes daily for 30 years but stopped after her stroke. Blood pressure is 125/70 mm Hg and pulse is 74/min and regular. Neurologic examination shows hemianesthesia of the right side and mild athetosis of the right hand. There is hyperesthesia on the right side of the body, as demonstrated by exaggerated pain on light touch. Motor strength is normal in all extremities. Which of the following is the most probable location of the stroke experienced by this patient 4 weeks ago?
This patient's stroke 4 weeks ago resulted in sensation deficits without motor weakness, cortical signs, or cranial nerve deficits (ie, pure sensory stroke). As numbness improved, she developed allodynia (burning pain) and hyperesthesia in areas impacted by the stroke (right arm and leg). These findings are likely due to the development of thalamic pain syndrome, a central neuropathic pain syndrome that can develop after a stroke impacting the thalamus (most likely a lacunar stroke); the adjacent basal ganglia can also be impacted, resulting in athetosis (writhing movements) or ballistic movements, as in this patient.
The thalamus relays sensory information between various subcortical areas and the somatosensory cortex. Thalamic pain syndrome, characterized by severe paroxysmal burning pain over affected areas, is classically exacerbated by light touch (allodynia). Because they develop in stroke-impacted areas, symptoms are typically unilateral. Sometimes, pain is triggered by other sensory modalities (eg, sound, taste).
(Choice A) Stroke impacting the internal capsule typically leads to motor deficits (alone or with sensory deficits) from disruption of the corticospinal fibers in the posterior limb. Although possible, a pure sensory stroke very rarely originates from the internal capsule. In addition, central poststroke pain syndrome is not characteristic.
(Choice B) Brainstem strokes commonly present with crossed signs of contralateral weakness with ipsilateral cranial nerve deficits. Because the oculomotor nerve [CN III] is located in the midbrain, strokes in this area typically present with ipsilateral CN III palsy and contralateral hemiparesis (from damage to the cerebral peduncle). Ataxia is also typically present due to damage to the superior cerebellar peduncle.
(Choice C) Infarction of the somatosensory cortex in the postcentral gyrus can cause sensory loss but does not typically impact the arm and leg equally due to the vascular supply relating to the somatotopic organization of the brain. However, if the stroke is large enough to impact the arm and leg, it would also likely be accompanied by hemiparesis (from primary motor cortex injury) and cortical signs (eg, aphasia, visual changes, neglect). A central poststroke pain syndrome is not characteristic.
(Choice D) Putaminal hemorrhage almost always involves the adjacent internal capsule, leading to contralateral hemiparesis and hemianesthesia (from disruption of corticospinal and somatosensory fibers in the posterior limb) and conjugate gaze deviation toward the side of the lesion (from damage to frontal eye field efferents in the anterior limb).
Educational objective:
Lacunar stroke of the posterolateral thalamus typically presents with sudden-onset contralateral sensory loss involving all sensory modalities (ie, pure sensory stroke). Weeks to months later, patients can develop thalamic pain syndrome characterized by severe paroxysmal burning pain over the affected area that is exacerbated by light touch (allodynia).