localising the lesion: “where in the cns”

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?