1. Case synthesis and localization: does the clinical picture match the imaging?
2. Etiology work-up for posterior circulation stroke: left V3 vertebral block, vertebral dissection, cardioembolism, small vessel disease.
3. Acute management: thrombolysis or thrombectomy eligibility, BP targets, antiplatelets, statin.
4. Complications of cerebellar infarct: edema, hydrocephalus, neurosurgical triggers, monitoring.
5. Vertebral artery stenosis or occlusion: medical therapy versus stenting.
6. Comorbidities: IHD post-PTCA, hypertension, and the unclear "RA" and "IDA" abbreviations.
7. Cervical MRI findings (C5-C7 root compression): relevance or incidental.
8. Secondary prevention, rehabilitation, and the foot injury history.

• Localization. A 62-year-old hypertensive man with IHD has acute imbalance, headache for 3 days, and left-sided weakness. MRI shows multifocal acute non-haemorrhagic infarcts in the cerebellum, bilateral on the latest note. The medicine unit also found a severe block in the left vertebral artery (V3 segment). This is a posterior circulation stroke, and the vertebral artery lesion is the likely source, either by artery-to-artery embolism or hypoperfusion.
• A mismatch to resolve. Cerebellar infarcts usually cause ipsilateral ataxia, vertigo, and vomiting, not dense hemiparesis. Your power grading of 1/5 in the left upper limb and 2/5 in the left lower limb, with a left extensor plantar, suggests corticospinal tract involvement. That points to brainstem (medullary or pontine) extension or a separate supratentorial or cord lesion. Review the DWI sequences for brainstem, PICA/AICA, or thalamic involvement. The mild C5-C7 root compression would not explain hemiparesis. The 3 days of headache also raise the question of vertebral artery dissection.
• Acute management. Onset was at 9:30 AM on 4 November, so check the time window first. Eligibility for IV thrombolysis depends on the arrival time and whether there is a disabling deficit. With BP 180/90, permissive hypertension is usual unless thrombolysis is given (then below 185/110 before, below 180/105 after). Otherwise, dual antiplatelet therapy for a short period is typical for minor stroke, with a high-intensity statin. For cerebellar strokes, serial neuro checks and a repeat CT at 24 to 48 hours help catch swelling and hydrocephalus early.
• Unclear abbreviations. I can't tell what "RA" and "IDA" mean in your note. "RA" could be rheumatoid arthritis or an atrial rhythm problem, and "IDA" could be iron deficiency anemia. This matters because atrial fibrillation would change anticoagulation, and anemia would change the work-up. Please clarify.

1. Case synthesis and localization: does the clinical picture match the imaging?
2. Etiology work-up for posterior circulation stroke: left V3 vertebral block, vertebral dissection, cardioembolism, small vessel disease.
3. Acute management: thrombolysis or thrombectomy eligibility, BP targets, antiplatelets, statin.
4. Complications of cerebellar infarct: edema, hydrocephalus, neurosurgical triggers, monitoring.
5. Vertebral artery stenosis or occlusion: medical therapy versus stenting.
6. Comorbidities: IHD post-PTCA, hypertension, and the unclear "RA" and "IDA" abbreviations.
7. Cervical MRI findings (C5-C7 root compression): relevance or incidental.
8. Secondary prevention, rehabilitation, and the foot injury history.

• Localization. A 62-year-old hypertensive man with IHD has acute imbalance, headache for 3 days, and left-sided weakness. MRI shows multifocal acute non-haemorrhagic infarcts in the cerebellum, bilateral on the latest note. The medicine unit also found a severe block in the left vertebral artery (V3 segment). This is a posterior circulation stroke, and the vertebral artery lesion is the likely source, either by artery-to-artery embolism or hypoperfusion.
• A mismatch to resolve. Cerebellar infarcts usually cause ipsilateral ataxia, vertigo, and vomiting, not dense hemiparesis. Your power grading of 1/5 in the left upper limb and 2/5 in the left lower limb, with a left extensor plantar, suggests corticospinal tract involvement. That points to brainstem (medullary or pontine) extension or a separate supratentorial or cord lesion. Review the DWI sequences for brainstem, PICA/AICA, or thalamic involvement. The mild C5-C7 root compression would not explain hemiparesis. The 3 days of headache also raise the question of vertebral artery dissection.
• Acute management. Onset was at 9:30 AM on 4 November, so check the time window first. Eligibility for IV thrombolysis depends on the arrival time and whether there is a disabling deficit. With BP 180/90, permissive hypertension is usual unless thrombolysis is given (then below 185/110 before, below 180/105 after). Otherwise, dual antiplatelet therapy for a short period is typical for minor stroke, with a high-intensity statin. For cerebellar strokes, serial neuro checks and a repeat CT at 24 to 48 hours help catch swelling and hydrocephalus early.
• Unclear abbreviations. I can't tell what "RA" and "IDA" mean in your note. "RA" could be rheumatoid arthritis or an atrial rhythm problem, and "IDA" could be iron deficiency anemia. This matters because atrial fibrillation would change anticoagulation, and anemia would change the work-up. Please clarify.

• Cord infarct. There is a short intramedullary T2/STIR hyperintensity at C2-C3 with diffusion restriction and no contrast enhancement. This is an acute upper cervical cord infarct. A demyelinating or inflammatory lesion would usually enhance, so the lack of enhancement argues against myelitis.
• Link to the vertebral artery. The upper cervical cord is supplied by branches of the vertebral arteries, which feed the anterior and posterior spinal arteries. The severe left V3 block (the segment that runs from C2 up to the atlas) fits as the source of both the cerebellar and the cord infarcts.
• Weakness and plantar response. A lesion at C2-C3 gives upper motor neuron weakness on the same side below the lesion. That fits left-sided weakness (power 1/5 left arm, 2/5 left leg) with an extensor left plantar. The imbalance comes from the cerebellar infarcts.
• Degenerative changes. The C5-C7 disc-osteophyte complexes only abut the nerve roots, and the canal diameters are within normal limits. The cord signal change is at C2-C3, away from these levels, so the spondylosis is probably incidental and does not explain the hemiparesis.
• Timing. Today is 9 November, day 5 after onset, so thrombolysis and thrombectomy are no longer options.

• Dissection or atherosclerosis. The 3 days of headache before the deficit fits dissection. A CTA or MRA of head and neck, with fat-suppressed T1 MRI of the neck, can tell the two apart. Management differs, mainly in how aggressively to stent and which antithrombotic to use.
• Cardiac source. The "newly detected RA" is unclear to me. If it means atrial fibrillation or flutter, anticoagulation becomes the central decision. If it means rheumatoid arthritis, it points to a different set of risk factors. I'm also unsure what "IDA" means here, possibly iron deficiency anemia. Please clarify both.
• Neurological risk. Cerebellar swelling can compress the brainstem or cause hydrocephalus, and an upper cervical cord lesion can threaten breathing. Both need monitoring.
• BP. 180/90 on arrival is in the permissive range, but later targets depend on vessel imaging.

1. Vertebral artery anatomy and why a V3 block causes both cerebellar and cord infarcts
2. Spinal cord infarction: clinical syndromes, imaging, differentials
3. Etiology work-up: dissection versus atherosclerosis versus cardioembolism
4. Antithrombotic and risk-factor management (antiplatelets, statin, BP, anticoagulation)
5. Vertebral artery stenosis: stenting versus medical therapy
6. Cerebellar infarct complications and monitoring
7. Rehabilitation and prognosis for cord infarct
8. Clarifying the "RA" and "IDA" entries and comorbidities (IHD post-PTCA)

1. Case synthesis and localization: does the clinical picture match the imaging?
2. Etiology work-up for posterior circulation stroke: left V3 vertebral block, vertebral dissection, cardioembolism, small vessel disease.
3. Acute management: thrombolysis or thrombectomy eligibility, BP targets, antiplatelets, statin.
4. Complications of cerebellar infarct: edema, hydrocephalus, neurosurgical triggers, monitoring.
5. Vertebral artery stenosis or occlusion: medical therapy versus stenting.
6. Comorbidities: IHD post-PTCA, hypertension, and the unclear "RA" and "IDA" abbreviations.
7. Cervical MRI findings (C5-C7 root compression): relevance or incidental.
8. Secondary prevention, rehabilitation, and the foot injury history.

• Localization. A 62-year-old hypertensive man with IHD has acute imbalance, headache for 3 days, and left-sided weakness. MRI shows multifocal acute non-haemorrhagic infarcts in the cerebellum, bilateral on the latest note. The medicine unit also found a severe block in the left vertebral artery (V3 segment). This is a posterior circulation stroke, and the vertebral artery lesion is the likely source, either by artery-to-artery embolism or hypoperfusion.
• A mismatch to resolve. Cerebellar infarcts usually cause ipsilateral ataxia, vertigo, and vomiting, not dense hemiparesis. Your power grading of 1/5 in the left upper limb and 2/5 in the left lower limb, with a left extensor plantar, suggests corticospinal tract involvement. That points to brainstem (medullary or pontine) extension or a separate supratentorial or cord lesion. Review the DWI sequences for brainstem, PICA/AICA, or thalamic involvement. The mild C5-C7 root compression would not explain hemiparesis. The 3 days of headache also raise the question of vertebral artery dissection.
• Acute management. Onset was at 9:30 AM on 4 November, so check the time window first. Eligibility for IV thrombolysis depends on the arrival time and whether there is a disabling deficit. With BP 180/90, permissive hypertension is usual unless thrombolysis is given (then below 185/110 before, below 180/105 after). Otherwise, dual antiplatelet therapy for a short period is typical for minor stroke, with a high-intensity statin. For cerebellar strokes, serial neuro checks and a repeat CT at 24 to 48 hours help catch swelling and hydrocephalus early.
• Unclear abbreviations. I can't tell what "RA" and "IDA" mean in your note. "RA" could be rheumatoid arthritis or an atrial rhythm problem, and "IDA" could be iron deficiency anemia. This matters because atrial fibrillation would change anticoagulation, and anemia would change the work-up. Please clarify.The cervical MRI changes the picture. The C2-C3 finding explains the left-sided weakness that the cerebellar infarct alone did not.

• Cord infarct. There is a short intramedullary T2/STIR hyperintensity at C2-C3 with diffusion restriction and no contrast enhancement. This is an acute upper cervical cord infarct. A demyelinating or inflammatory lesion would usually enhance, so the lack of enhancement argues against myelitis.
• Link to the vertebral artery. The upper cervical cord is supplied by branches of the vertebral arteries, which feed the anterior and posterior spinal arteries. The severe left V3 block (the segment that runs from C2 up to the atlas) fits as the source of both the cerebellar and the cord infarcts.
• Weakness and plantar response. A lesion at C2-C3 gives upper motor neuron weakness on the same side below the lesion. That fits left-sided weakness (power 1/5 left arm, 2/5 left leg) with an extensor left plantar. The imbalance comes from the cerebellar infarcts.
• Degenerative changes. The C5-C7 disc-osteophyte complexes only abut the nerve roots, and the canal diameters are within normal limits. The cord signal change is at C2-C3, away from these levels, so the spondylosis is probably incidental and does not explain the hemiparesis.
• Timing. Today is 9 November, day 5 after onset, so thrombolysis and thrombectomy are no longer options.

• Dissection or atherosclerosis. The 3 days of headache before the deficit fits dissection. A CTA or MRA of head and neck, with fat-suppressed T1 MRI of the neck, can tell the two apart. Management differs, mainly in how aggressively to stent and which antithrombotic to use.
• Cardiac source. The "newly detected RA" is unclear to me. If it means atrial fibrillation or flutter, anticoagulation becomes the central decision. If it means rheumatoid arthritis, it points to a different set of risk factors. I'm also unsure what "IDA" means here, possibly iron deficiency anemia. Please clarify both.
• Neurological risk. Cerebellar swelling can compress the brainstem or cause hydrocephalus, and an upper cervical cord lesion can threaten breathing. Both need monitoring.
• BP. 180/90 on arrival is in the permissive range, but later targets depend on vessel imaging.

1. Vertebral artery anatomy and why a V3 block causes both cerebellar and cord infarcts
2. Spinal cord infarction: clinical syndromes, imaging, differentials
3. Etiology work-up: dissection versus atherosclerosis versus cardioembolism
4. Antithrombotic and risk-factor management (antiplatelets, statin, BP, anticoagulation)
5. Vertebral artery stenosis: stenting versus medical therapy
6. Cerebellar infarct complications and monitoring
7. Rehabilitation and prognosis for cord infarct
8. Clarifying the "RA" and "IDA" entries and comorbidities (IHD post-PTCA)

1. Mechanism: one lesion, two territories

• A severe left V3 vertebral block can cause both the cerebellar infarcts and the C2-C3 cord infarct. The mechanisms are artery-to-artery embolism or low flow. The upper cervical cord is fed by vertebral artery branches.
• The cord lesion explains the left hemiparesis and extensor plantar. The cerebellar lesions explain the imbalance.
• Headache is a common early symptom of cerebellar infarction. Dissection should be considered, mainly in younger patients, but also when there is neck or head pain before the deficit (Plum and Posner's Diagnosis and Treatment of Stupor and Coma, Cerebellar Infarction section). At 62 with hypertension and IHD, atherosclerosis is more likely, but dissection is not excluded.

2. Work-up still worth completing

• Vessel imaging. CTA or MRA of head and neck, plus fat-suppressed T1 of the neck, to tell atherosclerotic stenosis from dissection. Also check the other vertebral artery, because a dominant or hypoplastic side changes risk, and check for bilateral disease.
• Cardiac source. ECG and prolonged rhythm monitoring (Holter or longer), plus echocardiography. This is why the "RA" entry matters. If it means atrial fibrillation or flutter, anticoagulation becomes the key decision, with timing based on infarct size. Please confirm.
• Labs. Lipid profile, HbA1c, CBC, and iron studies if "IDA" means iron deficiency anemia. Add ESR/CRP if rheumatoid arthritis is the intended meaning.
• Spine. The cord infarct does not need further spinal imaging unless the clinical picture changes. Vascular imaging should include the cervical segments.

3. Treatment framework

• Antithrombotic.
  • Short-course dual antiplatelet therapy (aspirin plus clopidogrel for 21 days) was proven in minor stroke or high-risk TIA. This patient has severe weakness (1/5 and 2/5), so he is not a "minor stroke" case, and he is past the 24-hour window. Single antiplatelet therapy is the safe baseline. Any DAPT choice would be a team decision.
  • If the cause is dissection, antiplatelet or anticoagulant therapy for at least 3 to 6 months is acceptable.
  • If AF is confirmed, start anticoagulation, delayed according to infarct size.
• Statin. Atorvastatin 40 to 80 mg, aiming for LDL below 70 mg/dL.
• BP. He has been past the first 24 to 72 hours, so BP can be lowered gradually. The long-term goal is below 130/80 mmHg. Avoid abrupt drops, because a tight vertebral stenosis makes perfusion pressure-dependent.
• Vertebral stenting. It is generally reserved for recurrent events despite optimal medical therapy. It is not first-line.
• Avoid neck manipulation and extreme rotation while the V3 lesion is being assessed.

4. Monitoring and complications

• Cerebellar edema. It develops gradually over 2 to 3 days after the infarct (Plum and Posner, Cerebellar Infarction section). He is now on day 5, so the peak risk is mostly past, but any drowsiness, new vomiting, or cranial nerve change needs urgent CT and neurosurgical review for hydrocephalus or brainstem compression.
• Upper cervical cord lesion. Watch breathing (vital capacity, cough), swallowing (bedside screen before oral feeding), and bladder function. Use DVT prophylaxis, pressure care, and early physiotherapy.
• Swallowing and aspiration. Check for dysphagia and dysarthria, which suggest medullary involvement.

5. Rehabilitation and prognosis

• Start early physiotherapy, occupational therapy, and gait training. Cerebellar ataxia often improves over weeks to months.
• Spinal cord infarcts are less predictable. Recovery depends on the severity at the start, and the 1/5 left arm power is a poor early marker. Re-examine at regular intervals.
• Counsel on adherence to antihypertensive and antiplatelet therapy, and on a farm worker's return-to-work needs.

6. Recent evidence check

7. Open points to confirm

• What "RA" and "IDA" mean in this note.
• The arrival time and whether any reperfusion decision was made.
• The result of vessel imaging for dissection versus atherosclerosis.
• The NIHSS at admission and the current neurological trend.

PubMed results: spinal cord infarction with vertebral artery occlusion

Closest match to your patient

• A 69-year-old hypertensive, diabetic man had an acute right PICA-territory cerebellar infarct and a C2-C4 cervical cord infarct.
• Cause: atherosclerotic occlusion of the right vertebral artery origin, with collateral flow through the deep cervical artery on angiography.
• CSF protein was mildly raised, with no cells and negative AQP4/MOG antibodies, which excluded inflammatory or demyelinating disease.
• He was treated with aspirin and rosuvastatin and improved within 2 weeks. Only headache was scored, so the improvement in cord function is not quantified.
• The authors attribute both infarcts to haemodynamic compromise in the PICA and spinal artery territories.

Systematic review (dissection)

• Mean age was about 40 years. Neck pain or headache occurred in 88%, a sensory level in 76%, and Brown-Séquard syndrome in 53%.
• The infarcts were mainly at C2-C5.
• Territories involved: spinal sulcal artery 42%, posterior spinal artery 29%, anterior spinal artery watershed 29%.
• 65% had a good outcome and 35% a poor one, with one death.
• Poor outcome was linked to smoking, age over 50, and anterior spinal artery watershed infarction. Sulcal artery infarction predicted a good outcome.

Other relevant reports

• Fujii et al. 2012 (PMID 22790805): a 73-year-old man had a right cerebellar infarct and right vertebral artery occlusion. Cord changes appeared on MRI a day later, at C5-C6. The authors suggest chronic cervical cord compression from spondylosis made the cord vulnerable to a unilateral vertebral occlusion. The first MRI showed cord compression without signal change, and the infarct appeared on the next day's scan. Your patient also has spondylosis, so a repeat cord MRI could be reasonable if new signs appear.
• Posterior unilateral cord infarction from dissection: Richard 2014, Bergqvist 1997, Jiang, Ann Neurol 2023, and Ouyang, Neurology 2022 with bilateral dissection. Posterior spinal artery territory infarcts typically cause an ipsilateral deficit, which matches your patient's left-sided weakness.
• Brown-Séquard and Horner: Ginos 2015. Check your patient for ipsilateral Horner syndrome and for sensory loss, because they would help localize the cord lesion.
• Treatment: Wu 2020 (PMID 29323631) used endovascular tirofiban in the acute stage. It is a single case, so it is not a basis for practice.
• Iatrogenic cord infarcts: Sarto 2021 after vertebral artery trapping, and Tsuruta 2018 after embolization. These are relevant if stenting or endovascular treatment of the vertebral artery is ever considered.

How this applies to your patient

1. Concurrent cerebellar and cervical cord infarcts from a vertebral artery lesion are documented but rare. His pattern matches the published case, and a single mechanism is the most likely explanation.
2. In the 17-case dissection series, neck pain or headache was nearly universal. His 3 days of headache therefore raises dissection, so vessel wall imaging (fat-suppressed T1) is worth doing alongside CTA or MRA.
3. In the atherosclerotic case, medical therapy with antiplatelet and statin was used and the patient did well. This is one case, so it cannot guide dosing or duration.
4. His risk factors for a poor outcome from the review are age over 50 and a severe initial deficit (1/5 left arm). I don't know his smoking status; the history lists "addiction-nil".

1. Case synthesis and localization: does the clinical picture match the imaging?
2. Etiology work-up for posterior circulation stroke: left V3 vertebral block, vertebral dissection, cardioembolism, small vessel disease.
3. Acute management: thrombolysis or thrombectomy eligibility, BP targets, antiplatelets, statin.
4. Complications of cerebellar infarct: edema, hydrocephalus, neurosurgical triggers, monitoring.
5. Vertebral artery stenosis or occlusion: medical therapy versus stenting.
6. Comorbidities: IHD post-PTCA, hypertension, and the unclear "RA" and "IDA" abbreviations.
7. Cervical MRI findings (C5-C7 root compression): relevance or incidental.
8. Secondary prevention, rehabilitation, and the foot injury history.

• Localization. A 62-year-old hypertensive man with IHD has acute imbalance, headache for 3 days, and left-sided weakness. MRI shows multifocal acute non-haemorrhagic infarcts in the cerebellum, bilateral on the latest note. The medicine unit also found a severe block in the left vertebral artery (V3 segment). This is a posterior circulation stroke, and the vertebral artery lesion is the likely source, either by artery-to-artery embolism or hypoperfusion.
• A mismatch to resolve. Cerebellar infarcts usually cause ipsilateral ataxia, vertigo, and vomiting, not dense hemiparesis. Your power grading of 1/5 in the left upper limb and 2/5 in the left lower limb, with a left extensor plantar, suggests corticospinal tract involvement. That points to brainstem (medullary or pontine) extension or a separate supratentorial or cord lesion. Review the DWI sequences for brainstem, PICA/AICA, or thalamic involvement. The mild C5-C7 root compression would not explain hemiparesis. The 3 days of headache also raise the question of vertebral artery dissection.
• Acute management. Onset was at 9:30 AM on 4 November, so check the time window first. Eligibility for IV thrombolysis depends on the arrival time and whether there is a disabling deficit. With BP 180/90, permissive hypertension is usual unless thrombolysis is given (then below 185/110 before, below 180/105 after). Otherwise, dual antiplatelet therapy for a short period is typical for minor stroke, with a high-intensity statin. For cerebellar strokes, serial neuro checks and a repeat CT at 24 to 48 hours help catch swelling and hydrocephalus early.
• Unclear abbreviations. I can't tell what "RA" and "IDA" mean in your note. "RA" could be rheumatoid arthritis or an atrial rhythm problem, and "IDA" could be iron deficiency anemia. This matters because atrial fibrillation would change anticoagulation, and anemia would change the work-up. Please clarify.The cervical MRI changes the picture. The C2-C3 finding explains the left-sided weakness that the cerebellar infarct alone did not.

• Cord infarct. There is a short intramedullary T2/STIR hyperintensity at C2-C3 with diffusion restriction and no contrast enhancement. This is an acute upper cervical cord infarct. A demyelinating or inflammatory lesion would usually enhance, so the lack of enhancement argues against myelitis.
• Link to the vertebral artery. The upper cervical cord is supplied by branches of the vertebral arteries, which feed the anterior and posterior spinal arteries. The severe left V3 block (the segment that runs from C2 up to the atlas) fits as the source of both the cerebellar and the cord infarcts.
• Weakness and plantar response. A lesion at C2-C3 gives upper motor neuron weakness on the same side below the lesion. That fits left-sided weakness (power 1/5 left arm, 2/5 left leg) with an extensor left plantar. The imbalance comes from the cerebellar infarcts.
• Degenerative changes. The C5-C7 disc-osteophyte complexes only abut the nerve roots, and the canal diameters are within normal limits. The cord signal change is at C2-C3, away from these levels, so the spondylosis is probably incidental and does not explain the hemiparesis.
• Timing. Today is 9 November, day 5 after onset, so thrombolysis and thrombectomy are no longer options.

• Dissection or atherosclerosis. The 3 days of headache before the deficit fits dissection. A CTA or MRA of head and neck, with fat-suppressed T1 MRI of the neck, can tell the two apart. Management differs, mainly in how aggressively to stent and which antithrombotic to use.
• Cardiac source. The "newly detected RA" is unclear to me. If it means atrial fibrillation or flutter, anticoagulation becomes the central decision. If it means rheumatoid arthritis, it points to a different set of risk factors. I'm also unsure what "IDA" means here, possibly iron deficiency anemia. Please clarify both.
• Neurological risk. Cerebellar swelling can compress the brainstem or cause hydrocephalus, and an upper cervical cord lesion can threaten breathing. Both need monitoring.
• BP. 180/90 on arrival is in the permissive range, but later targets depend on vessel imaging.

1. Vertebral artery anatomy and why a V3 block causes both cerebellar and cord infarcts
2. Spinal cord infarction: clinical syndromes, imaging, differentials
3. Etiology work-up: dissection versus atherosclerosis versus cardioembolism
4. Antithrombotic and risk-factor management (antiplatelets, statin, BP, anticoagulation)
5. Vertebral artery stenosis: stenting versus medical therapy
6. Cerebellar infarct complications and monitoring
7. Rehabilitation and prognosis for cord infarct
8. Clarifying the "RA" and "IDA" entries and comorbidities (IHD post-PTCA)I went ahead and covered the practical points for this patient, since the topic question didn't go through. Nothing below replaces the treating team's judgment.

1. Mechanism: one lesion, two territories

• A severe left V3 vertebral block can cause both the cerebellar infarcts and the C2-C3 cord infarct. The mechanisms are artery-to-artery embolism or low flow. The upper cervical cord is fed by vertebral artery branches.
• The cord lesion explains the left hemiparesis and extensor plantar. The cerebellar lesions explain the imbalance.
• Headache is a common early symptom of cerebellar infarction. Dissection should be considered, mainly in younger patients, but also when there is neck or head pain before the deficit (Plum and Posner's Diagnosis and Treatment of Stupor and Coma, Cerebellar Infarction section). At 62 with hypertension and IHD, atherosclerosis is more likely, but dissection is not excluded.

2. Work-up still worth completing

• Vessel imaging. CTA or MRA of head and neck, plus fat-suppressed T1 of the neck, to tell atherosclerotic stenosis from dissection. Also check the other vertebral artery, because a dominant or hypoplastic side changes risk, and check for bilateral disease.
• Cardiac source. ECG and prolonged rhythm monitoring (Holter or longer), plus echocardiography. This is why the "RA" entry matters. If it means atrial fibrillation or flutter, anticoagulation becomes the key decision, with timing based on infarct size. Please confirm.
• Labs. Lipid profile, HbA1c, CBC, and iron studies if "IDA" means iron deficiency anemia. Add ESR/CRP if rheumatoid arthritis is the intended meaning.
• Spine. The cord infarct does not need further spinal imaging unless the clinical picture changes. Vascular imaging should include the cervical segments.

3. Treatment framework

• Antithrombotic.
  • Short-course dual antiplatelet therapy (aspirin plus clopidogrel for 21 days) was proven in minor stroke or high-risk TIA. This patient has severe weakness (1/5 and 2/5), so he is not a "minor stroke" case, and he is past the 24-hour window. Single antiplatelet therapy is the safe baseline. Any DAPT choice would be a team decision.
  • If the cause is dissection, antiplatelet or anticoagulant therapy for at least 3 to 6 months is acceptable.
  • If AF is confirmed, start anticoagulation, delayed according to infarct size.
• Statin. Atorvastatin 40 to 80 mg, aiming for LDL below 70 mg/dL.
• BP. He has been past the first 24 to 72 hours, so BP can be lowered gradually. The long-term goal is below 130/80 mmHg. Avoid abrupt drops, because a tight vertebral stenosis makes perfusion pressure-dependent.
• Vertebral stenting. It is generally reserved for recurrent events despite optimal medical therapy. It is not first-line.
• Avoid neck manipulation and extreme rotation while the V3 lesion is being assessed.

4. Monitoring and complications

• Cerebellar edema. It develops gradually over 2 to 3 days after the infarct (Plum and Posner, Cerebellar Infarction section). He is now on day 5, so the peak risk is mostly past, but any drowsiness, new vomiting, or cranial nerve change needs urgent CT and neurosurgical review for hydrocephalus or brainstem compression.
• Upper cervical cord lesion. Watch breathing (vital capacity, cough), swallowing (bedside screen before oral feeding), and bladder function. Use DVT prophylaxis, pressure care, and early physiotherapy.
• Swallowing and aspiration. Check for dysphagia and dysarthria, which suggest medullary involvement.

5. Rehabilitation and prognosis

• Start early physiotherapy, occupational therapy, and gait training. Cerebellar ataxia often improves over weeks to months.
• Spinal cord infarcts are less predictable. Recovery depends on the severity at the start, and the 1/5 left arm power is a poor early marker. Re-examine at regular intervals.
• Counsel on adherence to antihypertensive and antiplatelet therapy, and on a farm worker's return-to-work needs.

6. Recent evidence check

7. Open points to confirm

• What "RA" and "IDA" mean in this note.
• The arrival time and whether any reperfusion decision was made.
• The result of vessel imaging for dissection versus atherosclerosis.
• The NIHSS at admission and the current neurological trend.

Closest match to your patient

• A 69-year-old hypertensive, diabetic man had an acute right PICA-territory cerebellar infarct and a C2-C4 cervical cord infarct.
• Cause: atherosclerotic occlusion of the right vertebral artery origin, with collateral flow through the deep cervical artery on angiography.
• CSF protein was mildly raised, with no cells and negative AQP4/MOG antibodies, which excluded inflammatory or demyelinating disease.
• He was treated with aspirin and rosuvastatin and improved within 2 weeks. Only headache was scored, so the improvement in cord function is not quantified.
• The authors attribute both infarcts to haemodynamic compromise in the PICA and spinal artery territories.

Systematic review (dissection)

• Mean age was about 40 years. Neck pain or headache occurred in 88%, a sensory level in 76%, and Brown-Séquard syndrome in 53%.
• The infarcts were mainly at C2-C5.
• Territories involved: spinal sulcal artery 42%, posterior spinal artery 29%, anterior spinal artery watershed 29%.
• 65% had a good outcome and 35% a poor one, with one death.
• Poor outcome was linked to smoking, age over 50, and anterior spinal artery watershed infarction. Sulcal artery infarction predicted a good outcome.

Other relevant reports

• Fujii et al. 2012 (PMID 22790805): a 73-year-old man had a right cerebellar infarct and right vertebral artery occlusion. Cord changes appeared on MRI a day later, at C5-C6. The authors suggest chronic cervical cord compression from spondylosis made the cord vulnerable to a unilateral vertebral occlusion. The first MRI showed cord compression without signal change, and the infarct appeared on the next day's scan. Your patient also has spondylosis, so a repeat cord MRI could be reasonable if new signs appear.
• Posterior unilateral cord infarction from dissection: Richard 2014, Bergqvist 1997, Jiang, Ann Neurol 2023, and Ouyang, Neurology 2022 with bilateral dissection. Posterior spinal artery territory infarcts typically cause an ipsilateral deficit, which matches your patient's left-sided weakness.
• Brown-Séquard and Horner: Ginos 2015. Check your patient for ipsilateral Horner syndrome and for sensory loss, because they would help localize the cord lesion.
• Treatment: Wu 2020 (PMID 29323631) used endovascular tirofiban in the acute stage. It is a single case, so it is not a basis for practice.
• Iatrogenic cord infarcts: Sarto 2021 after vertebral artery trapping, and Tsuruta 2018 after embolization. These are relevant if stenting or endovascular treatment of the vertebral artery is ever considered.

How this applies to your patient

1. Concurrent cerebellar and cervical cord infarcts from a vertebral artery lesion are documented but rare. His pattern matches the published case, and a single mechanism is the most likely explanation.
2. In the 17-case dissection series, neck pain or headache was nearly universal. His 3 days of headache therefore raises dissection, so vessel wall imaging (fat-suppressed T1) is worth doing alongside CTA or MRA.
3. In the atherosclerotic case, medical therapy with antiplatelet and statin was used and the patient did well. This is one case, so it cannot guide dosing or duration.
4. His risk factors for a poor outcome from the review are age over 50 and a severe initial deficit (1/5 left arm). I don't know his smoking status; the history lists "addiction-nil".

1. Why he has left hemiparesis (what the record supports)

• The MRI shows a C2-C3 intramedullary lesion with diffusion restriction and no enhancement, which is an acute cervical cord infarct.
• A lesion in the upper cervical cord damages the corticospinal tract on that side. The tract has already crossed in the lower medulla, so the weakness appears on the same side as the lesion, below it. A left cord lesion therefore gives left arm and leg weakness with a left extensor plantar.
• The arm is weaker than the leg (1/5 versus 2/5). At the upper cervical level the arm fibres lie close to the central grey matter, so a central or paracentral infarct can hit the arm more.
• The left V3 vertebral block fits as the source. The vertebral arteries feed the anterior and posterior spinal arteries to this cord segment.
• The cerebellar infarcts add imbalance and make walking worse. They do not cause weakness this dense.

2. Why the cervical spondylosis does not explain it

3. Why quadriparesis could be present or develop

1. Bilateral cord involvement. An anterior spinal artery territory infarct, or the "owl's eye" pattern (bilateral anterior horn signal), affects both sides. Bilateral cord infarcts are reported with bilateral vertebral disease. A published case of right vertebral occlusion with cerebellar and C2-C4 cord infarcts shows this pairing (Hu et al., Medicine 2025). Another published case of cerebellar and cord infarction after right vertebral occlusion presented with bilateral arm weakness (Fujii et al. 2012).
2. Extension of the infarct. Cord infarcts can evolve in the first days, and a lesion that was unilateral on day 1 can spread. Repeat the MRI if weakness progresses.
3. Brainstem extension. A medullary or pontine infarct from the same vertebrobasilar disease. Look for dysphagia, dysarthria, diplopia, facial weakness, or drowsiness.
4. Cord edema or compression. Swelling at the infarct site, or spondylotic narrowing making the cord vulnerable, as proposed in Fujii's case.
5. Cerebellar edema compressing the brainstem. It peaks around days 2 to 3, so it is less likely on day 5, but it must not be missed.
6. Other causes. Hypotension from overtreating blood pressure with a tight vertebral stenosis, spinal shock with later spasticity, critical illness weakness, or electrolyte problems.

4. What I would check now

• Examination. Compare power in all four limbs, tone (flaccid early, spastic later), reflexes, sensory level, pinprick versus joint position, bladder and bowel function, and ipsilateral Horner syndrome.
• Breathing and swallowing. An upper cervical lesion can affect the diaphragm (C3-C5). Check vital capacity and bedside swallow.
• Imaging. Repeat MRI of brain and whole cervical cord with DWI if there is any change. Review the existing sequences for a bilateral "owl's eye" pattern.
• Vessels. CTA or MRA of head and neck to look at both vertebral arteries and the basilar artery.
• Blood pressure. Avoid sudden drops.

5. Caveat