Neurological symptoms

MOVEMENT DISORDERS
• Tremors
• rhythmic oscillating movement of extremities or head
• Types:
• Action Tremors- essential, familial, senile type
• tremors of posture or activity, disappearing with rest,
usually assymetrical, head are commonly involved but
legs are rarely affected, lower amplitude than
parkinsonism
• NO rigidity or bradykinesia, maybe relieved temporarily
with alcohol intake
• Neurological exam ___/Normal
• DDx: pheochromocytoma (increase catecholamines)
hyperthyroidism, toxins, amphetamines, lithium,
amytriptyline intake
• Resting tremor- Parkinsonism
• Gross: 3-7/ sec “pill rolling” resting tremor
that improves with movement
• higher age group, not relieved by alcohol
• PE: decreased facial expression, rigidity of
the limbs, shuffling gait, slow movement,
patient is depressed, may lead to dementia
• Intention tremor
• - due to cerebellar dysfunction
• Tardive dyskinesia
• - usually due to prolonged intake of neuroleptics
• Manifestations: oral-buccal-lingual dyskinesia ( e.g
tongue protrusion, lip smacking, facial grimacing) , may
involve limbs and trunks as well
• Hemiballismus
• Wild involuntary flinging of an extremity due to CVD
(Cerebrovascular) of subthalamic nuclei
• Acute dystonic posture (e.g. turning of neck)
• Usually caused by neuroleptic idiosyncrasy
• Myoclonus
• Shock-like non-patterned contraction of a muscle, entire
muscle or group of muscle secondary to anoxic brain
damage, epilepsy, degenerative disease
 WRITER’S CRAMP(A type of FOCAL DYSTONIA)
Patients describe a discomfort in the hand associated with use of excessive
force. Abnormal posturing is typical.
Example of patient’s script in writer’s cramp.
POST ANOXIC
DYSTONIA. Foot
posture.
POST
ANOXIC
DYSTONIA.
Secondary
callous.
TAR-
DIVE
DYSKI-
NESIA.
Various
form of
sponta-
neous
tongue
move
ment.
MS. Facial myokymia in its most extensive form causing narrowing of the palpebral
conjunctiva and slight elevation of the angle of the mouth. Facial myokymia consist of
fine unilateral flickering movement of the muscle that maybe confined to one area of the
face or maybe present throughout the facial nerve distribution.
BLEPHAROSPASM.This disease produces excessive blinking to the
point where the eye becomes permanently closed
OCCULOGYRIC CRISIS
SPASMODIC
TORTICOLIS. A
characteristic
head posture.
Contraction of
the left
sternomastoid is
particularly
prominent.
 ATAXIA
• Disorder of coordination and rhythm
• Locate the lesion
• Frontal lobe lesion
• Tumors (meningioma, glioma, metastatic tumor)
• Sign of cerebellar dse (fronto-ponto-cerebellar pathways
• Staggering gait, alternating pronation supination test (APST),
nystagmus (tends to fall backwards[frontal lesion])
• Perseveration, grasp & suck reflex, incontinence & slowness of
mentation
• Headache is common, dementia maybe present
• Anterior cerebral artery syndrome
• -also affects frontal lobe
• -aneurysm of ant communicating artery may affect frontal lobe
• Hydrocephalus
• -enlarged frontal horns of lateral ventricle affects leg fibers and may
produce ataxia (plus me
• Subcortical Lesions
• Mechanism: involvement of
corticocerebellar connections and
pyramidal tract dysfunction
• Multiple strokes (‘etat lacunaire)
• -ataxia, emotional labilities, brisk reflexes
(increased jaw jerk), dysarthria, dementia
• Brainstem Lesions
• Mechanism: involvement of cerebellar
tracts
• Most common cause of ataxia secondary
to brainstem lesions: CVA, multiple
sclerosis
• Brainstem signs
• -crossed motor & sensory findings
• -internuclear ophthalmoplegia
• -nystagmus
• -dysarthria
• Cerebellar Lesion
• Mechanism: direct involvement of coordination
pathways
• Signs: limb, trunk, gait & speech ataxia,
nystagmus, hypotonia
• Causes :
• Cerebellar haemorrhage, infarct, tumor
• -occipital headache and ocular gaze palsies
• -Normal limb strength and sensation
• -tumors seen in children, rare in adults
• -metastatic tumors in adult
• Spinocerebellar degeneration
• -the syndrome include olivo-ponto-cerebellar
degeneration & Friedrich’s ataxia
• -(+) family history and widespread nervous
system involvement (e.g. peripheral
neuropathy, upgoing toes, etc)
• Alcoholism or occult malignancy
• -associated with cerebellar degeneration
• -alcoholic degeneration (ataxia of gait and
of legs, less prominent involvement of
arms, speech and ocular motility,
associated with polyneuropathy)
• -Wernicke’s encephalopathy (acute ataxia
and oculomotor paralysis associated with
alcoholism, responds well to thiamine)
• Spinal Cord Lesion
• Mechanism: ataxia via the posterior column dysfunction, involvement of
spinocerebellar tracts or spasticity from involvement of pyramidal
tracts)
• (+) Romberg’s test - indicates posterior column disease
• Cervical spondylosis with associated cervical myelopathy
• -(+) neck and arm pain
• -there maybe posterior column dysfunction and upgoing toes
(pyramidal tract involvement)
• Multiple Sclerosis
• -often involves spinal cord
• -other CNS lesion + (+) history of previous attacks
• Vitamin B12 deficiency
• -combined system disease (e.g. involvement of posterior and lateral
columns of spinal cord
• -general weakness and paresthesias which lead to leg stiffness & ataxia
• -loss of position and vibration sense associated with upgoing toes +
decreased or absent knee and ankle jerks secondary to peripheral
neuropathy
• -see mental changes
• Other causes of ataxia secondary to spinal cord dysfunction
• Spinal cord tumor, spinocerebellar degeneration, syringomyelia, tabes
dorsalis, amyotrophic lateral sclerosis
• Peripheral Nerve Lesion
• -ataxia secondary to weakness and in idiopathic
polyneuritis due to dorsal root involvement
• Idiopathic polyneuritis (Guillain-Barre Syndrome)
• -may present as ataxia in early stage
• Dx: absent reflex, increased CSF protein, slow
nerve conduction time
• Muscular Lesion
• Ataxia secondary to muscular weakness
• Myopathy - acquired: polymyositis, thyroid
myopathy
• Congenital: muscular dystrophy (Duchene’s)
• Acute forms: drug or chemical ingestion (alcohol,
lead), acute labyrinthitis, postictal states (after
seizures), LE
 AGNOSIA
• Object recognition
• AGNOSIA – defect of recognition of simple objects in the
presence of adequate primary sensory perception
• visual agnosia – failure of visual recognition of an
object, due to a lesion in the visual association area
(area adjacent to the calcarine occipital cortex),
– visuospatial agnosia – if he cannot revisualize familiar places
such as his home and cannot maintain orientation in a previously
known environment.
– finger agnosia – inability to identify own fingers (due to a lesion
of the angular gyrus and frequently forms a part of
GERTSMANN’s syndrome – finger Agnosia, Allochiria (right-left
disorientation), Agraphia and Acalculia.
• tactile agnosia (astereognosis) – inability to
recognize objects by palpatation, due to a
lesion of the posterior parietal lobe.
– autotopagnosia – loss of appreciation or
identification of a body part in which the patient may
fail to identify his own limb or even one side of the
body, it is a lesion of the parietal lobe, demonstrated
by willingness of the patient to accept the examiner’s
hand or arm as his own.
– anosognosia – implies denial of disease due to loss
of perception of the affected part, usually a paralyzed
limb, due to a frontal & parietal lobe lesion of the
non-dominant hemisphere.
• auditory agnosia – inability to perceive the
meaning of sound despite the absence of
deafness.
 APRAXIA
• Praxis – inability to execute a planned
motor action, in the absence of paralysis.
• There are three stages considered in the
development of a skilled act: the
development of an idea of movement,
formulation of the plan of its execution,
and finally, motor performance of the plan
(basis of the three types of apraxia)
• Ideational apraxia – due to lesion in the
supramarginal gyrus of the parietal lobe,
no impairment of motor mov’t but idea is
confused, ex. Request px. To light
cigarette, px. Fails to take cigarette out of
the package.
• Ideamotor apraxia – occurs when there is
interface with the transmission of the
appropriate impulses transcortically to the
motor centers to convert the idea into
coordinated motor action, seen in diffused
cortical disease ex. Patient is unable to
carry out the desired action like lick
protrude the tongue upon request.
• Motor apraxia – failure to perform a series
of finer skilled movements on request in
the absence of weakness or paralysis,
planned mov’t involving limbs as a whole is
intact, lesion is in the pre-motor frontal
cortex on the opposite side to the affected
limb, there is loss of dexterity in handling
small objects or performing rapid finger
movements.
DRESSING APRAXIA. Typically associated with lesion of the non dominant
parietal lobe.
END OF LECTURE