localising the lesion: “where in the cns”
DESCRIPTION
Localising the lesion: “where in the CNS”. Kate Hassan. Learning objectives. Definition of CNS and PNS Definition of UMN and LMN Function of each of the cerebral lobes The homunculus Circle of willis and blood supply to the cerebral hemispheres Motor tracts – lateral corticospinal - PowerPoint PPT PresentationTRANSCRIPT
LOCALISING THE LESION: “WHERE IN THE CNS”Kate Hassan
LEARNING OBJECTIVES Definition of CNS and PNS Definition of UMN and LMN Function of each of the cerebral lobes The homunculus Circle of willis and blood supply to the
cerebral hemispheres Motor tracts – lateral corticospinal Sensory tracts – lateral spinothalamic and
dorsal columns Stroke syndromes Clinical case scenarios
DEFINITIONS CNS = Brain and spinal cord PNS = anything outside brain and spinal cord
Also include autonomic nervous system and cranial nerves
MOTOR CONTROL SYSTEMS Corticospinal (pyradmial)
Skilled, intricate, strong and organised movements Defectiveness loss of skilled voluntary movement,
spasticity and reflex changes Extrapyradimal system
Fast, fluid movements that the corticospinal system has generated
Defectiveness bradykinesia, rigidity, tremor, chorea The cerebellum
Co-ordinating smooth and learned movement initiated by the pyradimal system and in posture and balance control
Defectiveness ataxia, past pointing, action tremor and incoordination
CORTICOSPINAL (PYRADIMAL) SYSTEM
THE HOMUNCULUS
DEFINITION OF UMN AND LMN
UMN SIGNS VS LMN SIGNS
UMN LMNwastingfasciculationtonePowerreflexesPlantars
UMN LMNwasting nofasciculationtonePowerreflexesPlantars
UMN LMNwasting no yesfasciculationtonePowerreflexesPlantars
UMN LMNwasting no yesfasciculation notonePowerreflexesPlantars
UMN LMNwasting no yesfasciculation no yestonePowerreflexesPlantars
UMN LMNwasting no yesfasciculation no yestone increasedPowerreflexesPlantars
UMN LMNwasting no yesfasciculation no yestone increased decreasedPowerreflexesPlantars
UMN LMNwasting no yesfasciculation no yestone increased decreasedPower decreasedreflexesPlantars
UMN LMNwasting no yesfasciculation no yestone increased decreasedPower decreased increasedreflexesPlantars
UMN LMNwasting no yesfasciculation no yestone increased decreasedPower decreased increasedreflexes increasedPlantars
UMN LMNwasting no yesfasciculation no yestone increased decreasedPower decreased increasedreflexes increased decreasedPlantars
UMN LMNwasting no yesfasciculation no yestone increased decreasedPower decreased increasedreflexes increased decreasedPlantars up going
UMN LMNwasting no yesfasciculation no yestone increased decreasedPower decreased increasedreflexes increased decreasedPlantars up going down going
SENSORY PATHWAYS Peripheral nerves carry sensation from dorsal
roots to the cord Posterior columns (dorsal columns)
Vibration, joint position, light touch and point discrimination
Cross in the brainstem passing to the thalamus Spinothalamic tracts
Pain and temperature Cross within the cord and pass in the spinothalamic
tracts to the thalamus and reticular formation Sensory cortex
Fibres from the thalamus pass to the parietal region sensory cortex and motor cortex
CEREBRAL LOBES
CORTICAL FUNCTIONS Frontal lobe
Reasoning, planning, parts of speech, movement, emotions and problem solving
Left frontal = broccas area (aphasia) Parietal lobe
Movement, orientation, recognition, perception of stimuli Occipital lobe
Visual processing Temporal lobe
Perception and recognition of auditory stimuli, memory and speech
Left temporal = wernicke’s area Cerebellum
Balance and co-ordination Basal ganglia
Initiation and inhibition of movement
QUIZ Patient has difficulty walking and slurred speech
Cerebellum Patients wife reported personality change and
difficulty wording what they wanted to say Frontal lobe
Patient has difficulty recognising objects and often gets lost unable to find their way home Parietal and occipital lobe
Patient has difficulty remembering significant past events and no longer enjoys listening to music Temporal lobe
STROKE SYNDROMES TACS = total anterior circulation syndrome PACS = partial anterior circulation syndrome POCS = posterior circulation syndrome LACS = lacunar syndrome
STROKE TACS – All three of
Hemiplegia or hemi sensory loss Visual field defect Disturbance of higher function
Dysphasia Dysphagia
PACS – 2 out of 3 LACS – blockage of small branch of big artery
No visual field defect Pure motor stroke Pure sensory Sensory motor Ataxia
POCS – brain stem, cerebellum, cranial nerves Bilateral motor or sensory Conjugate eye movement disorder Cerebeller dysfunction Hemiplegia or cortical blindness
STROKE Acute occlusion of blood vessel leading to
hypoxia and infarction Risk factors
DM, hypertension, smoking, hypercholesterolemia, FHx, AF
Investigations bloods, CT, MRI, carotid dopplers, Echo, ECG, 24
hour tape Treatment in ischaemic stroke
Aspirin Clopidogrel Supportive management
CEREBELLAR SYNDROME Causes
Vascular lesion Alcohol Demyelination Tumours Hypothyroidism Metabolic disorders
Signs “DANISH” Dysdiadochokinesis Ataxia Nystagmus Intention tremor Slurred speech, dysarthria Hpyotonia, hyporeflexia
MULTIPLE SCLEROSIS Areas of demyelination and perivascular inflammation
(white plaques) Disseminated in time and occurring anywhere within
CNS Aetiology - ?autoimmune ?vitamin D deficiency Classification
Benign Relapse remitting Secondary chronic progressive Primary progressive
Investigations LP – increased protein, increased immunoglobulin,
oligoclonal bands Visual evoked potentials MRI
MULTIPLE SCLEROSIS On examination
Unsteady gait Reduced proprioception Brisk reflexes
Brown-sequard syndrome Loss of movement on same side as damage Loss of pain and temp and sensation on opposite side
Management Symptoms control (tremors, pain, muscle spasms) steroids Beta-inferons Glatiramer IV natalizumab
MOTOR NEURONE DISEASE Degeneration of upper and lower motor neurones of
unknown cause 5-10% autosomal dominant Types
Spinal muscular atrophy – limb weakness due to involvement of spinal cord anterior horn cells
Primary later sclerosis – spastic limb weakness due to UMN involvement of the spinal cord
Progressive bulbar palsy – involvement of bulbar motor neurones, progressive disease
Amyotrophic lateral sclerosis – mixture of all the above Investigations
Diagnosed clinically after other causes excluded EMG confirms fasciculation's and fibrillations
Management – symptom control Fatal within 3-5 years
MOTOR NEURONE DISEASE Cardiac and smooth muscle aren’t involved
and ocular muscle very rarely Autonomic dysfunction occurs late Signs
Dysarthria, brisk jaw reflex Fasciculation/wasting in deltoids, biceps,
quadriceps and in tongue Weakness in all4 limbs, brisk reflexes in arms,
absent in legs Combination of UMN and LMN
CLINICAL CASE 1 23, female presents to her GP with a 2 week
history of bilateral leg weakness having started with pins and needles and numbness in her hands and feet. She has had a few days of urinary incontinence which has resolved. 2 years ago she had an episode of blurred vision and pain in the right eye which lasted a month and fully resolved
CASE 1 What is the most likely diagnosis? What other signs or symptoms might you see
in this condition? What is the pathological basis of this
disorder? What further investigations would you do? How would you manage this patient?
CLINICAL CASE 2 61 female Becoming increasingly weak on her right side
over a one week period. She is unable to walk and has slurred speech and right side of her face is drooping
Past history of breast cancer o/e – right facial weakness, grade 4/5
weakness of the right arm and leg, right homonymous hemianopia and some difficulty naming objects and reflexes are brisk on the right side and her right plantar response is upgoing
CASE 2 What is the likely diagnosis?
CASE 2 CT head shows extensive oedema
surrounding the subtle impression of a ring enhanced lesion in the left frontal lobe, extending into the left parietal lobe. There is associated mass effect displacing the lateral ventricle
CASE 2 What is the likely cause? Other features that may be present? What management options are available?
CASE 3 76 male Background of AF (on warfarin) has 2 hour
history of severe global right sided weakness. He is eye-opening to painful stimuli and is moving his left side spontaneously. When questioned he seems confused
CASE 3 What is his GCS? What is the diagnosis? What investigations would you do? What are the important risk factors? How wound you manage this patient?
CASE 4 56 male 6 month history of progressive weakness of
his right hand. Also had problems with swallowing and has choked whilst eating on several occasions
o/e he has wasting of his upper and lower limbs and some fasciculation's were noted his right plantar was up going and his reflexes were generally brisk
CASE 4 Diagnosis? What investigations would you perform? How would you manage this patient?
THANK YOU FOR LISTENINGAny questions?