Lesions and Disorders Flashcards
Cerebellar lesions produce…
Dysmetria (movements that are inaccurate in space and disjointed in time)
Think that this is because the cerebellum’s major function is to enable smooth, coordinated movement (sort of like Tai Chi).
Tetanus toxin
Fill in, from spinal cord chapter
Lower motor nerve lesions
With few exceptions, these result in flaccid paralysis ipsilateral to and at the level of the lesions.
Other symptoms include hyporeflexia, hypotonicity, fasciculations, atropy (wasting) of the affected motor units, and fibrillations.
Poliomyelitis
Fill in
UMN lesion
Result in spastic (i.e. hypertonic,stiff) paresis (wakness) that may be ipsilateral, or contralateral, to the lesion, and below the level of the lesion.
Will result in hyperreflexia.
Horner’s Syndrome
Results in the following signs ipsilateral to the lesion:
Meiosis
Ptosis
Anhydrosis
Also results in orthostatic/postural hypotension
Is due to a lesion that interferes with autonomic axons in the hypothalamic tract and/or the sympathetic chain.
Uncal Herniation
In the event of increased intracranial pressure, uncal herniation can cause descending contralateral motor problems via compression of the cerebral peduncle.
CN III may also be compressed (signs include CN III palsy, ptosis, and dilated/”blown” pupil)
CN III Palsy
Results in loss of function all the muscles that control the eye except for the SO and LR muscles -> this leads to a “down-and-out” eye (external strabismus).
Knocks out the levator palpabrae superioris -> drooping eyelid (ptosis)
Loss of the autonomic innervation of the pupil constrictor muscle, the sphincter pupillae -> blown/constitutively dilated pupil (myadrasis)
CN VI Palsy
This results in internal strabismus (inwardly deviated eye)
Patients present with diplopia
Hemiparesis
Fill in
Bell’s Palsy
Idiopathic unilateral facial paralysis
Loss of the function of muscles of facial expression on the side ipsilateral to lesion due to a cranial nerve VII lesion (Facial nerve lesion)
What is the difference between a central and a peripheral Bell’s Palsy?
The forehead muscles receive mixed innervation from both facial nerves.
Therefore, of the lesion to the facial nerve occurs above the level of the isolated facial nerve, it is a central facial palsy, where the paralysis is only below the level of the forehead).
Peripheral facial palsy results in paralysis of the entire side of the lesion that is ipsilateral to the lesion.
Upper (superior) homonomous quadrantanopsia
“Pie in the sky” scotoma.
Results from lesions to (contralateral?) Meyer’s loop.
Which region of the brain is pathologic in Parkinson’s disease?
Destruction of the dopaminergic neurons in the substantia nigra pars compacta,(SNc) leads to dopamine depletion and consequent strong inhibition of the thalamus and movement.
Which region of the brain is pathologic in Huntington’s disease?
The striatum
Movement disorders
Conditions characterized by abnormal voluntary movements or by the presence of excessive involuntary movements.
Can have hyper- or hypo-kinetic features.
What types of dysfunctions do movement disorders reflect?
Dysfunction:
- among basal ganglial structures
- between the basal ganglia, cerebellum, and other CNS areas.
What are the four major symptoms of parkinsonism?
- Bradykinesis (hypokinesis)
- rest tremor
- postural instability
- rigidity
(TBP R) -> tau beta pi recruitment
(tremor, bradykinesis, postural instability, rigidity)
Hypokinetic movement disorders
Too few, too small, too slow
All have a core of “parkinsonism,” i.e. bradykinesis/akinesia and rigidity.
PD and other causes of parkinsonism (multiple systems atrophy, progressive supranuclear palsy).
Hyperkinetic movement disorders
Too much, too big, too fast
May be jerky (myoclonus, chorea, ballism, tics), or not-jerky (dystonia, athetosis, tremor)
Grestmann’s Syndrome
Left parietal lesion of the “angular gyrus”.
Results in “body schema disturbance” (Autopagnosia), although the four following signs are typical:
- agraphia
- finger agnosia
- acalculia
- R/L confusion
Balint’s Syndrome
Disorder of reaching and looking.
Due to bilateral parietal lesions.
Can arise from the tau-opathies, prion disease, etc.
What are the most common symptoms of Balint’s syndrome?
Optic ataxia
Ocular apraxia
Simultagnosia
Broca’s aphasia
This is expressive aphasia, in that the patient knows what they want to say but cannot produce the words.
These patients speak in a non-fluent(slow), telegraphic, agrammatical way.
Their repetiting, comprehension, and naming are usually not significantly impaired. However, since they have impaired understanding of grammar, their comprehension may be diminished if the meaning depends on a complex grammatical structure.
Global aphasia
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Which cortical area is lesioned in expressive aphasia?
Focal lesion in Broca’s area (Broadmann’s area 44/45, the posterior inferior frontal gyrus), which is important for the production or expression of concepts.
Which region of the brain is lesioned in receptive aphasia?
Focal lesion in Wernicke’s area (posterior section of the superior temporal gyrus), which is the area involved in understanding written and spoken language
Which cortical area is lesioned in conductive aphasia?
The arcuate fasciculus, which connects Broca’s area with Wernicke’s area
What usually causes a discrete aphasia?
Small, focal, branch artery stroke due to small emboli.
These lead to Broca’s, Wernicke’s, and Conductive aphasias.
What usually causes a global aphasia?
Carotid occlusion due to atherosclerosis.
What is the main problem that patients with semantic dementia face?
The concepts underlying objects become slowly degraded, so eventually they lose the ability to name, understand, and use all objects except those that are very personal to them (i.e. their personal coffee cup or tooth brush).
How would a patient with right hemisphere language disorder present?
- impaired prosody
- poor comprehension of metaphor, humor
- limited grasp of extended discourse
- disorganized, tangential discourse
Parkinson’s Disease
Progressive, degenerative disorders of the brain affecting dopaminergic neurons.
Major symptoms common to all forms of parkinsonism (TBPR), with minor symptoms.
Minor Sx of Parkinson’s Disease
- masked face
- micrographia
- dysautonomia (?): urinary incontinence, orthostatic hypotension, constipation
- dystonia
- hypophonia
- RBD (REM behavior disroder)
- Cognitive/affective
Pathology of PD
Loss of pigmented neurons in the substantia nigra with glial proliferation, microglial inflammation, and Lewy bodies with alpha-synuclein in neurons.
What do Lewy body look like in an H&E and what are they composed of?
Hallmark of PD
Round, eosinophillic cytoplasmic inclusions of alpha-synuclein protein in pigmented (dopaminergic?) neurons.
Atypical parkinsonian syndromes
- Multiple systems atrophi
- Progressive supranuclear palsy
- Corticobasal degeneration
- Wilson’s disease
What are hallmarks of multiple systems atrophy in addition to parkinsonian features?
Autonomic failure (ex. severe orthostatic hypotension.
MSA is a form of atypical parkinsonian syndrome.
What are hallmarks of progressive supranuclear palsy in addition to parkinsonian features?
- Opthalmoparesis (abnormal eye movements) -> no real voluntary control of eye movements
- “Surprised” expression
PSP is a form of atypical parkinsonian syndrome.
What are hallmarks of corticobasal degeneration in addition to parkinsonian features?
- Apraxia
- Dystonia
Corticobasal degeneration is a form of atypical parkinsonian syndrome.
What are hallmarks of Wilson’s disease in addition to parkinsonian features?
- Young onset
- Dystonia
Wilson’s disease is a form of atypical parkinsonian syndrome.
TREATABLE: use chelating agents
Broca’s aphasia
Patients know what they want to say, but cannot get it out.
Speech is non-fluent (telegraphic, agrammatic, slow) and repetition and naming are impaired. Comprehension, however, is preserved, unless the comprehension of a word involves extracting meaning from a complex syntax or grammatical structure.
Above which spinal cord segment will you know get Horner’s syndrome with complete cord transection?
T1.
Aphasias are always _____ phenomena.
Cortical
Three causes of sudden onset neurological deficit in brain/cortex:
- Vascular (ischemia)
- Seizure
- Migraine
Why do UMN lesions result in hyperreflexia?
The hyperactive muscle stretch reflexes seen in patients with UMN lesions is mainly due to a loss of inhibition of gamma motor neurons by reticulospinal medullary UMNs.
RECALL: UMN systems have a net overall inhibitory effect on muscle stretch and inverse muscle stretch reflexes.
Poliomyelitis
RESULTS FROM: loss of LMNs in the ventral horn caused by the polio-virus.
FEATURES: Typical to LMN lesion symptoms.
Multiple sclerosis
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Amyotropic lateral sclerosis (ALS)
Combined anterior horn cell-pyramidal tract syndrome
Tabes dorsalis (Posterior Column Syndrome)
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Syringomyelia
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Brown-Sequard syndrome
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Anterior spinal artery occlusion
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Subacute Combined Degeneration
Posterolateral Column Syndrome
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Complete cord transection
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