Case Vignettes in Neurology

PATIENT CASE STUDIES

Case 7 2/19 Vertigo
Case discussion A 44-year old male, previously healthy without a history of hypertension, diabetes, rode on a high speed roller coaster along with his two teenage children while on vacation in Florida. Shortly after alighting from the ride he developed sudden onset of severe posterior left sided neck pain. His symptoms progressed and an hour later he developed "dizziness" severe nausea with vomiting. He did not have visual or motor symptoms. There was no history of alcohol. He rested in bed. On awakening the next morning the nausea and neck pain persisted. He felt that he was spinning when he attempted to rise out of bed and he had numbness on the left side of face. On examination he was afebrile; BP was 160/95, pulse 98/min regular. There was moderate cervical paraspinal muscle spasm with tenderness. There were no carotid bruits. He was alert, attentive, oriented x 3, speech was fluent, with good memory for recent events. On attempting to draw the face of a clock he had minor difficulty with the right side of his diagram. On formal visual confrontational perimetry he had difficulty recognizing the presence of small objects on the right side. Extraocular movements were full. There was horizontal, jerk type, nystagmus more marked on looking to the right. The nystagmus did not have a latency period with positional testing, did not fatigue with repetitive testing, and was not abolished with visual fixation. Hearing was intact. There was decreased sensation and blink on corneal testing on the left side and there was mild subjective reduction in sensation to pin prick on the left side of the face. Motor examination was normal. DTRs were symmetric. Plantar reflexes were flexor. Sensory testing was intact to primary modalities. Cerebellar testing revealed mild dysdiadokinesis on the left upper extremity. Gait was ataxic.
Summarize the Case in 1-2 sentences. 44 y/o male with acute cervical paraspinal muscle spasm secondary to rollercoaster ride and possible whiplash injury presents one hour later with sudden onset of nausea/vomiting; horizontal jerky nystagmus; decreased pain, sensation and corneal reflex on left face; decreased ability to draw and recognize objects in right field of vision; dysdiadochokinesis; ataxic gait; and new onset hypertension. good Discuss lesion localization on the basis of the physical examination. The lesion can be localized to the cerebellopontine region of the brainstem and the distribution of the posterior cerebral artery, either the primary visual cortex of the occipital lobe or the posterior parietal lobe. The vertigo, nausea, vomiting, nystagmus (central vestibular type) and ataxic gait could all be d/t involvement of the vestibular nuclei and/or its fibers. Destruction of the sensory and motor fibers and/or nucleus of cranial nerve V account for the loss of pain, sensation and corneal reflex from the ipsilateral face. The ataxic gait could also be accounted for by cerebellar involvement, as could the dysdiadochokinesis. The apparent visual deficit may be d/t either a lesion in the left posterior visual radiations entering the occipital lobe or a lesion in the left posterior parietal lobe causing right constructional apraxia secondary to right hemispatial neglect; however, left-sided lesions of the parietal cortex causing hemispatial neglect is exceedingly rare, even in left-handed individuals. too long; try to list signs with accompanying localization; otherwise good Discuss underlying pathogenesis on the basis of clinical course. The focal neurologic deficits are acute in nature and are not progressive; the patient apears to be relatively stable at this point. The acute onset of the event, the clinical presentation and apparent multiple lesions point to vascular, traumatic or infectious causes. good Indicate one likely clinical diagnosis. List (or classify) alternative diagnoses. Most likely diagnosis is endothelial damage of vertebral arteries secondary to whiplash injury causing multiple emboli and subsequent infarction of the left cerebellum and brainstem at the level of the pons, as well as occipital or parietal cortical involvement. DDX includes traumatic fracture of the petrous temporal bone, compressing the cerebellopontine angle, and contrecoup lesion to the occipital/parietal cortex; or subdural hemorrhage overlying the occipital/parietal cortex causing increased ICP and herniation; or infectious embolization, such as from bacterial endocarditis. good, be brief however Indicate 2 ancillary tests that would assist in confirming or refuting the clinical diagnosis. Indicate the test results that would confirm the clinical diagnosis. MRI is the imaging study of choice for localization of CNS lesions in a stable patient, and it can also be used as MR angiography to visualize patency of the brain’s vascularization. The MRI would show a discolored area of infarction in the affected areas and show an absence of blood flow in occluded vessels supplying those areas. Additional tests should include a C-spine film to r/o cervical fracture as the cause of trauma to the vasculature. good (stick to the question, 2 answers mri and mra) Indicate complications of the disease and ancillary tests that would help evaluate them. Complications of CVA include risk of another embolic stroke, slow subarachnoid hemorrhage and subsequent slow increase of ICP resulting in herniation and death d/t compression of respiratory centers, and cerebral edema causing compression of adjacent structures, all of which could be evaluated by CT or MRI, and would be seen as a loss of symmetry and shift of midline structures. Both CT and MRI can be used to rule out increased ICP and herniation d/t subdural hemorrhage. Continuous ECG monitoring to rule out intermittent arrhythmias as a source of thrombotic emboli. Echocardiography to rule out endocarditis and infectious emboli, a patent foramen ovale, and akinetic myocardium. Lumbar puncture to rule out bacterial emboli and meningitis. I am not asking for the complications of CVA; I am asking for the complications of your main dx ie vertebral a. dissection. consequently endocarditis is not a complication. complicaitons may include focal neurological deficits in distal arterial territories, progression of thrombosis, distal embolization from thrombotic event Discuss how the underlying pathophysiology is relevant in the management of this patient. Management would include anticoagulation therapy to prevent further CVAs, especially if there is a history of rheumatic heart disease in which case anticoagulation therapy is indefinite. Aspirin and/or warfarin should be used, although there is a risk of hemorrhage with warfarin use. Antithrombolytic therapy is contraindicated in this patient d/t the amount of time between the event and the treatment; it is generally only used within three hours of acute onset of CVA symptoms. This is because after three hours the portion of the affected vessel distal to the occlusion is weakened and is likely to hemorrhage when flow is suddenly returned. Education about controlling blood pressure and cholesterol should be supplied. discuss the pathophysiology; note issues of maintaining CPP acutely and maintaining high BP; anticoagulation in this patient is a good idea but why? what is the rationale based on the likely pathophysiology (thrombosis secondary to a vertebral a. dissection); also mention pathophysiology of an ischemic infarct (see collins chapter on cerebrovascular disease)

Case 7 2/19 Vertigo

Case discussion

A 44-year old male, previously healthy without a history of hypertension, diabetes, rode on a high speed roller coaster along with his two teenage children while on vacation in Florida. Shortly after alighting from the ride he developed sudden onset of severe posterior left sided neck pain. His symptoms progressed and an hour later he developed "dizziness" severe nausea with vomiting. He did not have visual or motor symptoms. There was no history of alcohol. He rested in bed. On awakening the next morning the nausea and neck pain persisted. He felt that he was spinning when he attempted to rise out of bed and he had numbness on the left side of face.

On examination he was afebrile; BP was 160/95, pulse 98/min regular. There was moderate cervical paraspinal muscle spasm with tenderness. There were no carotid bruits. He was alert, attentive, oriented x 3, speech was fluent, with good memory for recent events. On attempting to draw the face of a clock he had minor difficulty with the right side of his diagram. On formal visual confrontational perimetry he had difficulty recognizing the presence of small objects on the right side. Extraocular movements were full. There was horizontal, jerk type, nystagmus more marked on looking to the right. The nystagmus did not have a latency period with positional testing, did not fatigue with repetitive testing, and was not abolished with visual fixation. Hearing was intact. There was decreased sensation and blink on corneal testing on the left side and there was mild subjective reduction in sensation to pin prick on the left side of the face. Motor examination was normal. DTRs were symmetric. Plantar reflexes were flexor. Sensory testing was intact to primary modalities. Cerebellar testing revealed mild dysdiadokinesis on the left upper extremity. Gait was ataxic.

Summarize the Case in 1-2 sentences.

44 y/o male with acute cervical paraspinal muscle spasm secondary to rollercoaster ride and possible whiplash injury presents one hour later with sudden onset of nausea/vomiting; horizontal jerky nystagmus; decreased pain, sensation and corneal reflex on left face; decreased ability to draw and recognize objects in right field of vision; dysdiadochokinesis; ataxic gait; and new onset hypertension.

good

Discuss lesion localization on the basis of the physical examination.

The lesion can be localized to the cerebellopontine region of the brainstem and the distribution of the posterior cerebral artery, either the primary visual cortex of the occipital lobe or the posterior parietal lobe. The vertigo, nausea, vomiting, nystagmus (central vestibular type) and ataxic gait could all be d/t involvement of the vestibular nuclei and/or its fibers. Destruction of the sensory and motor fibers and/or nucleus of cranial nerve V account for the loss of pain, sensation and corneal reflex from the ipsilateral face. The ataxic gait could also be accounted for by cerebellar involvement, as could the dysdiadochokinesis. The apparent visual deficit may be d/t either a lesion in the left posterior visual radiations entering the occipital lobe or a lesion in the left posterior parietal lobe causing right constructional apraxia secondary to right hemispatial neglect; however, left-sided lesions of the parietal cortex causing hemispatial neglect is exceedingly rare, even in left-handed individuals.

too long; try to list signs with accompanying localization; otherwise good

Discuss underlying pathogenesis on the basis of clinical course.

The focal neurologic deficits are acute in nature and are not progressive; the patient apears to be relatively stable at this point. The acute onset of the event, the clinical presentation and apparent multiple lesions point to vascular, traumatic or infectious causes.

good

Indicate one likely clinical diagnosis. List (or classify) alternative diagnoses.

Most likely diagnosis is endothelial damage of vertebral arteries secondary to whiplash injury causing multiple emboli and subsequent infarction of the left cerebellum and brainstem at the level of the pons, as well as occipital or parietal cortical involvement. DDX includes traumatic fracture of the petrous temporal bone, compressing the cerebellopontine angle, and contrecoup lesion to the occipital/parietal cortex; or subdural hemorrhage overlying the occipital/parietal cortex causing increased ICP and herniation; or infectious embolization, such as from bacterial endocarditis.

good, be brief however

Indicate 2 ancillary tests that would assist in confirming or refuting the clinical diagnosis. Indicate the test results that would confirm the clinical diagnosis.

MRI is the imaging study of choice for localization of CNS lesions in a stable patient, and it can also be used as MR angiography to visualize patency of the brain’s vascularization. The MRI would show a discolored area of infarction in the affected areas and show an absence of blood flow in occluded vessels supplying those areas.

Additional tests should include a C-spine film to r/o cervical fracture as the cause of trauma to the vasculature.

good (stick to the question, 2 answers mri and mra)

Indicate complications of the disease and ancillary tests that would help evaluate them.

Complications of CVA include risk of another embolic stroke, slow subarachnoid hemorrhage and subsequent slow increase of ICP resulting in herniation and death d/t compression of respiratory centers, and cerebral edema causing compression of adjacent structures, all of which could be evaluated by CT or MRI, and would be seen as a loss of symmetry and shift of midline structures. Both CT and MRI can be used to rule out increased ICP and herniation d/t subdural hemorrhage. Continuous ECG monitoring to rule out intermittent arrhythmias as a source of thrombotic emboli. Echocardiography to rule out endocarditis and infectious emboli, a patent foramen ovale, and akinetic myocardium. Lumbar puncture to rule out bacterial emboli and meningitis.

I am not asking for the complications of CVA; I am asking for the complications of your main dx ie vertebral a. dissection. consequently endocarditis is not a complication. complicaitons may include focal neurological deficits in distal arterial territories, progression of thrombosis, distal embolization from thrombotic event

Discuss how the underlying pathophysiology is relevant in the management of this patient.

Management would include anticoagulation therapy to prevent further CVAs, especially if there is a history of rheumatic heart disease in which case anticoagulation therapy is indefinite. Aspirin and/or warfarin should be used, although there is a risk of hemorrhage with warfarin use. Antithrombolytic therapy is contraindicated in this patient d/t the amount of time between the event and the treatment; it is generally only used within three hours of acute onset of CVA symptoms. This is because after three hours the portion of the affected vessel distal to the occlusion is weakened and is likely to hemorrhage when flow is suddenly returned. Education about controlling blood pressure and cholesterol should be supplied.

discuss the pathophysiology; note issues of maintaining CPP acutely and maintaining high BP; anticoagulation in this patient is a good idea but why? what is the rationale based on the likely pathophysiology (thrombosis secondary to a vertebral a. dissection); also mention pathophysiology of an ischemic infarct (see collins chapter on cerebrovascular disease)