Lesions Flashcards
Bulbar palsy clinical presentation
LMN weakness of muscles supplied by cranial nerves with cell bodies within the medulla: IX, X, XII
Tounge: wasted, flaccid, fasciculating, fast movements
Dysphagia?
Soft palate elevation?
Quiet, nasal speech?
Jaw jerk/gag reflex absent?
Pseudobulbar palsy clinical presentation
Bilateral UMN disease of medullary cranial nerves
Tongue: stiff/spastic, slow movements, no wasting
Dysphagia?
Normal soft palate elevation
Gravelly ‘donald duck’ speech / slurred high pitched dysarthria
Exaggerated jaw jerk
Mood disturbances
Causes of bulbar palsy
Degenerative: motor neurone disease Vascular: stroke Inflammatory: Guillain-barre Infective: botulism Neoplastic: brainstem tumours Congenital
Causes of pseudobulbar palsy
Degenerative: MND
Vascular: stroke
MS
Head trauma
Frontal cerebral hemisphere lesion presentation
Intellectual impairment, personality change
Urinary incontinence
Mono/hemiparesis
Broca’s aphasia (if left frontal)
Left temporo-parietal cerebral hemisphere lesion presentation (dominant hemisphere)
Agraphia: inability to write Alexia: word blindness Acalculia: inability to calculate Wernicke's aphasia Contralateral sensory neglect
Right temporo-parietal cerebral hemisphere lesion presentation
Failure of face recognition
Contralateral sensory neglect
Occipital cerebral hemisphere lesion presentation
Visual field defects
Visuospatial defects
Lateral cerebellar lesion presentation
Ipsilateral pathological signs
Broad, ataxic gait: test heel-toe walking, +ve Rhomberg test suggests sensory (rather than cerebellar) ataxia
Titubation: rhythmic head tremor
Dysarthria: slurred, staccato speech
Nystagmus: towards the side of the lesion
Dysmetric saccades: inability to change eye focus
Upward drift (if pronator drift also present = UMN pathology also)
Rebound phenomenon
Hypotonia: decreased in pure cerebellar disease
Mild hyporeflexia
Dysmetria: imprecise coordination
Dysdiadochokinesis: clumsy rapid alternating movements
Cerebellar examination investigations
Full neurological exam
TFTs
Antineuronal antibodies
MRI brain
Midline cerebellar lesion presentation
Rolling, broad, ataxic gait
Difficulty standing/sitting unsupported
Cannot perform Rhomberg’s with eyes open/closed
Vertigo/vomiting if extension into 4th ventricle
Causes of bilateral cerebellar dysfunction
Alcohol
Drugs: phenytoin, anti-epileptics
Paraneoplastic cerebellar degeneration: antineuronal antibodies present, common with breast/SCC of lung
Severe hypothyroidism
Causes of unilateral cerebellar dysfunction
MS
Stroke
Tumour: acoustic neuroma, meningioma
Components of the basal ganglia
Corpus striatum: caudate nucleus, globus pallidum, putamen
Subthalamic nucleus
Substantia nigra
Parts of the thalamus
Basal ganglia lesion presentation
Bradykinesia progressing to akinesia: slowness of movement/loss of power of voluntary movement
Muscle rigidity
Involuntary movements…
Tremor
Dystonia: spasms
Athetosis: writhing involuntary movements of hands/face/tongue
Chorea: jerky involuntary movements
Hemiballismus: violent involuntary movements, proximal muscles of one arm