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OUTLINE
Introduction Clinical features of neurological diseases Headaches Altered sensorium Vertigo Muscle weakness Movement disorders Higher cortical dysfunction Gait disturbance / imbalance Sensory abnormalities Common clinical scenarios
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INTRODUCTION
Important guide to radiological evaluation of neurologic disorders Inadequate clinical information can
greatly hamper accuracy/utility of radiological investigations result in inappropriate interventions increase mortality and morbidity Adverse financial consequences Litigation
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NEUROLOGICAL DX AETIOLOGIES
Vascular Infection / Inflammatory Trauma/Toxins Autoimmune Metabolic Idiopathic Neoplastic Psychogenic/Seizures Degenerative/Drugs Endocrine Congenital (VITAMINS DEC)
HEADACHE
Headache = pain in the head. Symptoms suggestive of serious underlying dx Worst headache ever
First severe headache Subacute worsening over days or weeks Abnormal neurological examination Fever or unexplained systemic signs Vomiting preceding headache HA induced by bending, lifting, cough Disturbance of sleep or HA immediately on awakening Known systemic illness e.g. malignancy Onset after age 55 years
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HEADACHE ii
Features of serious underlying causes of headache
Meningitis Generalized headache; associated nuchal rigidity; photophobia; may be febrile; focal signs Intracranial hemorrhage Severe headache; altered sensorium; seizures; nuchal rigidity in subarachnoid/intraventricular hrrhage; bloody tap or xanthochromia
Glaucoma
Pounding severe HA; associated nausea/vomiting/progressive altered sensorium; focal deficits; seizures Severe eye oain; nausea or vomiting; painful red eye
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ALTERED SENSORIUM
Coma (GCS<8)
Diffuse cortical dysfunction Brainstem reticular activating system dysfunction Causes: metabolic, structural intracranial abnormalities e.g. vascular, trauma, SOL Accompanying neurologic features aid definitive diagnosis
Drowsiness/ stupor: similar aetiology as coma Delirium/ acute confusional state: metabolic, vascular, trauma, toxic/drug induced
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VERTIGO
An illusory or hallucinatory sense of movement of the environment (sense of spinning) Can be physiologic or pathologic Pathologic causes:
Visual: new glasses; diplopia Somatosensory: peripheral neuropathy; myelopathy vestibular: labyrinthine dx; 8th nerve dx; central connections
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MUSCLE WEAKNESS
Reduction in normal power of one or more muscles -plegia: complete weakness -paresis: mild or moderate weakness Pattern UMN: corticospinal tract involvement brain or spinal cord LMN pattern: anterior horn cells, nerve roots, peripheral nerve Myopathic: muscle or NMJ; proximal weakness typically Distribution:
Hemi - one half of the body (corticospinal UMN) Para both legs (spinal cord or cortex; flaccid or spastic) Quadri all four limbs (UMN or LMN) Mono one limb (UMN or LMN)
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MUSCLE WEAKNESS
MUSCLE WEAKNESS
MOVEMENT DISORDERS
Disturbance of fluent movt or unintended extra movement Most have a biochemical rather than structural basal ganglia dx Classified as: hyperkinetic or hypokinetic Hemiballismus:
contralateral subthalamic nucleus lesion vascular, etc
Chorea:
acute/subacute toxins, drugs, pregnancy, hyperthyroidism, antiphospholipid syndrome, rheumatic fever Chronic; neurodegenerative dx e.g. Huntingtons disease
Myoclonus:
Metabolic and neurologic aetiologies Structural causes: brainstem or spinal lesions causing palatal or segmental myoclonus
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MOVEMENT DISORDERS
Tremor Rest tremor: maximal at rest (parkinsonian tremor) Postural tremor (max. with limb postured against gravity; DD acute: toxic/metabolic; insiduous: benign essential tremor Intention tremor (max. during voluntary movt towards a target; cause cerebellar disease) Parkinsonism Hypokinetic movt disorder Tremor, bradykinesia (slowness), rigidity, postural impairment) DD: PD, multiple system atrophies, PSP, vascular, drug/toxins, head trauma, etc
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Due to left hemispheric lesion in 90% of right handed, 60% left handed; small % no language dominance; right dominance in others (incl. small minority of right handed)
Causes: stroke, tumors, trauma, degenerative
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AGNOSIAS
Recognition deficits e.g. face (prosopagnosia), objects (visual object agnosia occipito-temporal region) due to bilateral posterior cerebral artery infarcts
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SENSORY ABNORMALITIES
Lesions at any level of neuraxis: parietal cortex, thalamus, brainstem, spinal cord, spinal root, peripheral nerve, etc Distribution and nature important for localization Parietal lobe: Contralateral hemineglect; abnormal higher sensory fxn, hemilateral loss of primary sensation (pseudothalamic) Focal sensory seizures Thalamus: Hemisensory disturbance from head to toe (e.g. stroke) Brainstem: Harlequin pattern ipsilateral facial sensory loss and contralateral body (lateral medulla) Contralateral face/arm/leg pons and midbrain NPMCN Radiology Update Course 2013
SENSORY ABNORMALITIES ii
Spinal cord: Distribution of the sensory abnormality and accompanying tract dysfunction is important Hemisection Contralat loss pain and temp below; ipsilat loss of proprioception and muscle power below Transection: sensory level on trunk Central canal (syrinx): sensory dissociation with loss of pain and temperature. Nerve and root: discrete boundaries of sensory abnormality
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VISUAL COMPLAINTS
Impaired visual acuity Visual field loss
Hemifield
Homonymous hemianopsia Quadrantanopia
Upper quadrant Lower quadrant
Bitemporal
Conjugate gaze
Disconjugate gaze (diplopia): cranial neuropathy; myopathy; neuromuscular junction; brainstem
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Stroke:
Abrupt onset Stepwise deterioration if any Subtype features: ischaemic; haemorrhagic (ICH v. SAH) Risk factor profile
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Seizures
Idiopathic or due to structural intracranial abnormalities
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