# Clinical Cases: Thalamus and Hypothalamus ## Case 1: Thalamic Stroke with Dejerine-Roussy Syndrome ### Patient Presentation **Demographics:** 72-year-old female with history of hypertension and atrial fibrillation **Chief Complaint:** Left-sided numbness followed by severe burning pain **History of Present Illness:** Three months ago, the patient experienced sudden onset of complete numbness affecting her entire left side including face, arm, and leg. She was evaluated in the emergency department where a CT head showed no hemorrhage and MRI revealed an acute infarct in the right thalamus (ventral posterolateral and ventral posteromedial nuclei). She was found to be subtherapeutic on warfarin and was transitioned to apixaban for stroke prevention. Over the following weeks, her numbness partially improved, but she developed progressively severe burning, stabbing pain throughout her left side that is constant and debilitating. Light touch, such as clothing brushing against her skin or bedsheets touching her leg, provokes excruciating pain. The pain interferes with sleep and has significantly impacted her quality of life. **Physical Examination:** - General: Appears uncomfortable, guarding left side - Mental status: Alert, oriented, no cognitive deficits - Cranial nerves: Intact - Motor: Strength 5/5 throughout, no drift - Sensory: - Left face, arm, and leg: Diminished light touch and pinprick sensation - Allodynia: Light touch produces severe pain throughout left hemibody - Proprioception mildly impaired on left - Right side: Normal sensation to all modalities - Reflexes: 2+ and symmetric, plantar responses flexor - Coordination: Intact **Workup:** - Original MRI brain: Right thalamic infarct involving VPL and VPM nuclei - Follow-up MRI: Chronic right thalamic infarct with encephalomalacia - CTA head and neck: No significant stenosis - Echocardiogram: Mild left atrial enlargement, no thrombus - INR: Subtherapeutic at time of stroke **Diagnosis:** Dejerine-Roussy syndrome (thalamic pain syndrome) secondary to right thalamic stroke **Treatment:** - Anticoagulation with apixaban for atrial fibrillation (stroke prevention) - Amitriptyline 25 mg at bedtime, titrated to 50 mg for central neuropathic pain - Gabapentin 300 mg three times daily added for additional pain control - Lamotrigine considered if insufficient response - Referral to pain management specialist - Physical therapy for desensitization techniques **Clinical Pearl:** Dejerine-Roussy syndrome occurs in approximately 8% of thalamic stroke patients. Initial sensory loss is followed weeks to months later by severe central neuropathic pain with allodynia. The ventroposterior nucleus of the thalamus is the key structure; damage disrupts the relay of sensory information and leads to maladaptive reorganization causing spontaneous pain and hypersensitivity. Treatment is challenging and often requires combination therapy with tricyclic antidepressants, anticonvulsants (gabapentin, pregabalin, lamotrigine), and sometimes opioids or neuromodulation. --- ## Case 2: Central Diabetes Insipidus ### Patient Presentation **Demographics:** 34-year-old male **Chief Complaint:** Excessive thirst and urination for 3 weeks following head injury **History of Present Illness:** The patient was involved in a motor vehicle collision 4 weeks ago, sustaining traumatic brain injury with brief loss of consciousness. CT at that time showed a small frontal contusion that was managed conservatively. He was discharged after 3 days. One week after discharge, he noticed he was drinking much more water than usual and urinating frequently, often waking 4-5 times per night to void. He estimates he is drinking 6-8 liters of water daily and producing large volumes of dilute urine. Despite the large fluid intake, he feels persistently thirsty. He has not had any fevers, dysuria, or other symptoms. He has no history of diabetes mellitus or psychiatric illness. **Physical Examination:** - Vital signs: BP 118/72, HR 78, Temp 37.0C - General: Well-appearing, no distress - HEENT: Mucous membranes slightly dry - Neurological: Alert, oriented, no focal deficits; cranial nerves intact including visual fields - Cardiovascular: Regular rate and rhythm - Skin: Decreased turgor **Workup:** - Serum sodium: 148 mEq/L (elevated) - Serum osmolality: 302 mOsm/kg (elevated, normal 275-295) - Urine osmolality: 85 mOsm/kg (inappropriately dilute) - Urine specific gravity: 1.002 - Random glucose: 95 mg/dL - Serum creatinine: 1.1 mg/dL - 24-hour urine volume: 9.2 liters - Water deprivation test: - After water deprivation: Urine osmolality remained 95 mOsm/kg despite serum osmolality rising to 298 mOsm/kg (failed to concentrate) - After desmopressin 2 mcg IV: Urine osmolality increased to 580 mOsm/kg (appropriate response to exogenous ADH) - MRI brain with pituitary protocol: Loss of posterior pituitary bright spot on T1; small residual frontal contusion; pituitary stalk appears normal **Diagnosis:** Central diabetes insipidus secondary to traumatic brain injury **Treatment:** - Desmopressin (DDAVP) 0.1 mg orally twice daily, with instructions to hold one dose if excessive water retention occurs - Serum sodium monitoring weekly initially, then monthly - Free access to water with instruction to drink to thirst - Endocrinology follow-up for anterior pituitary function assessment - Education regarding the need for lifelong therapy and medical alert identification **Clinical Pearl:** Central diabetes insipidus results from deficient ADH secretion from the hypothalamic-neurohypophyseal system. The water deprivation test differentiates central DI (responds to exogenous desmopressin) from nephrogenic DI (kidneys resistant to ADH). Loss of the posterior pituitary "bright spot" on T1 MRI reflects absence of stored ADH in the posterior pituitary. Post-traumatic DI may occur immediately after injury or develop over days to weeks, and some cases resolve spontaneously. The hypothalamus contains the supraoptic and paraventricular nuclei that produce ADH, which is transported to and released from the posterior pituitary. --- ## Clinical Image ![Thalamic stroke MRI](case_01_image.jpg) **Image Description:** Brain MRI demonstrating thalamic infarct. The thalamus serves as the relay station for sensory information traveling to the cerebral cortex. Damage to the ventroposterior nucleus causes contralateral hemisensory loss initially, followed by development of central neuropathic pain (Dejerine-Roussy syndrome) in many patients. **Attribution:** Image from Radiopaedia (https://radiopaedia.org/), Creative Commons Attribution-NonCommercial-ShareAlike 3.0 license.