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2. Motor unit
o Motor unit is the connection of LMN to group of muscle fibers (few to 100)
o Variations in force, range, rate and type of movements are related to the number
and size of the motor unit
o Muscles are innervated according to the segments of the spinal cord in a
metameric distribution
o Motor nerve fiber of each ventral root participate together with the neighboring
roots to the plexuses formation
o Each large muscle can be innervated by 2 or more roots
o But a single peripheral nerve innervates completely a muscle or a group of muscle
12. Most common etiology for primary generalized seizures with onset
in adolescence
o Juvenile Myoclonic Epilepsy
Most common etiology is: autosomal dominant genetic
o Juvenile absence seizure
o generalized tonic clonic seizures
13. 3 causes of epilepsy with onset over 60
o Vascular
o Metastatic
o Degenerative
o Infectious traumatic
o Metabolic
o Toxic
14. Lenticular nucleus part that controls the leg and the trunk
o Lenticular nucleus contains putamen and globus pallidus
o Putamen participates in control of limb and trunk movements
18. A motor and nonmotor sign of Parkinson that must be present for
positive diagnosis
Motor:
o Bradykinesia (MANDATORY)
o At least one of the following
Muscular rigidity
4-6 Hz rest tremor
postural instability not caused by primary visual,vestibular,
cerebellar, or
proprioceptive dysfunction
Non-motor:
-dementia, sensory symptoms, autonomic dysfunction, sleep disorders (REM behavor
disorders, insomnia), depression
37. 59 y.o. male hospitalized with acute onset of right hemiplegia 8 hrs
ago; CT shows hypodensity in deep & superficial territory of left
MCA. In 6 hrs pt has altered consciousness and right eye mydriasis.
Significance?
o The significance is that there isn’t any aphasia meaning that the nondominant area
is affected areas Wernicke and broca (comprehension and speech respectively)
are found in the dominant hemisphere only so if the patient was right handed the
occlusion of the left middle cerebral artery would have affected his speech
production
Non dominant lesions often cause visuospatial problems ,
inattention
Lesions of either side can be associated with a hemianopia
o initially, there may be depressed consciousness and deviation of gaze toward the
side of the lesion
o In right-handed people, occlusion of the left MCA produces global aphasia in
which the patient can neither understand the speech of others nor produce
meaningful speech
o In the nondominant hemisphere, unilateral neglect, anosognosia (unawareness of
the deficit), and spatial disorientation occur.
o Probably its an occlusion of M1 segment due to altered consciousness and right
hemiplegia plus there isn’t any aphasia so not m2 superior or inferior trunk
occlusion
42. How can internal carotid stenosis >90% cause ischemic stroke,
pathophysiology
o If collateral supply through the circle of willis is thrombosed or embolizes to
involve the MCA or its branches
o Carotid dissection
o Atheromatous plaque
51. Treatment for 35 y.o. with cavernous sinus thrombosis and dental
abscess
o Treat dental abscess with penicillin plus metronidazole
o Dental abscess predisposes to brain abscess
o Patient has Septic Cavernous Sinus Thrombosis
infection usually spreads from the paranasal sinuses, dental
abscesses, or other infections affecting the orbit or middle third of the
face. S. aureus is the most common organism.
Treatment
1. Blood cultures are often negative= delays in diagnosis
2. When diagnosis is established empirical antimicrobial treatment
may not provide full coverage
3. Prompt drainage of indentifiable source of infection as well as
specific antistaphylococcal agents
4. Heparin anticoagulation without a loading dose to reduce
morbidity from associated brain ischemia
a. It should be noted that experience in septic venous
thrombosis is limited compared with more frequent use of
anticoagulation in nonseptic venous thrombosis
5. Despite therapy mortality rates remain as high as 44%
78. Most Relevant clinical feature of an infarct in the cortical area of the
left anterior cerebral artery?
o cortical branches
it supplies the anterior 3/4 of the medial part of the frontal lobe
a superior strip of the lateral surface of the cerebral
hemispheres
anterior 4/5 of the corpus callosum
o occlusion distal to ant. Communicating artery = contralateral weakness and
cortical sensory loss in the leg
105. Type of MRI sequence that gives us information about the total
lesion load in the brain in MS? But for active lesions?
o Leakage of gandolinium serves as marker for inflamation due to breakdown of
blood brain barrier
o Demyelination seen through black holes on t2
o Flair sequence (fluid attenuated inversion recovery)hyperintensity
-nonvalvular A fib
-ventricular thrombus
-prostethic valve
-rheumatic heart disease
-acute MI
117. Define the brain concussion, the cerebral laceration and enumerate the
types of cerberal lacerations
- cerebral concussion.
a condition in which there is a traumatically induced alteration in mental status, with or without
an associated loss of consciousness (LOC)
_ A broader definition is a traumatically induced physiologic disruption in brain function that is
manifested by LOC, memory loss, alteration of mental state or personality, or focal neurologic
deficits
_ a primary posttraumatic effect
Signs and symptoms:
Confusion
Delayed responses and emotional changes
Pain/dizziness
Visual disturbances
Amnesia
Signs of increased intracranial pressure
120. What are the physiologic effects of the vestibulo-spinal pathway activity?
But of the reticulo-spinal pathway?
-Medial vestibulospinal tract-innervates neck mms and helps coordinate hear and eye movement
Lateral vestibulospinal tract- provides excitatory signals to interneurons, which relay the signal
to the motor neurons in antigravity muscles (extensor mm of legs that help with posture)
-reticulospinal tract- controls activity of alpha and gamma motor neurons; mediates pressor and
depressor effects on circulatory system; helps control breathing; works with vestiulosspinal tract
for coordinated mm flexion
121. What type of neurologic lesions may be the cause of unilateral hypotonia
in the the left inf limb?
-neocerebellum lesion
-tabetic neurosyphilis
-LMN lesion
122. Which are the possible localisation of the lesion in a patient with right
hemiparesis facial palsy?
LMN- peripheral lesion-facial nerve palsy
124. Describe the clinical picture of a patient with right spasmodic torticollis
associated with retrocollis?
Patient has head pulled back and right?
-spasmodic torticollis aka cervical dystonia
127. What treatment do you recomment for a patient with ischemic stroke and
atrial fibrosis for the secondary prevention of a recurrent stroke?
-Change lifestyle
-give oral anticoagulants: acenoccoumarol (warfarin, sintrom), direct thombin inhibitors,
inhibitors of Factor X activated (Rivaroxaban, apixaban)
-antiplatelets (clopidogrel, aspirin)
-revascularization (stenting, endarterectomy)
134. What are the main clinical and neuropsychological differences between a
mild neurocgnitive impairment and a major neurocognitive impairment,
according to the criteria od DSM-5?
Major neurocognitive disorder: evidence of significant cognitive declinefrom a previous level
ofperformance in oneor more of the domains outlined above based on concerns of the patient,a
knowledgeable informantor the clinician that there has been a significant decline in cognitive
function. AND the Mild Neurocognitive Disorder : Evidence of minor cognitive declinefrom a
previous level of performance in one or moreof the domains outlined above based on concerns of
the patient, a knowledgeable informant or the clinician that there has been a mild decline
incognitive function .
135. What is the clinical difference between ideational and ideomotor apraxia
when asking the patient to perform transtive gestures?
-ideomotor: patient has deficit in ability to plan or complete motor actions/gestures that rely on
somatic memory; unable to explain how to perform action but able to imagine or act out a
movement (eg burshing teeth); automatic-voluntary dissociation (cannot pick up a phone when
asked to but if it hears it ring it answers it)
-ideational:patients have inability to conceptualize a task and impaired ability to complete
multistep action; consists of inability to select and carry out an appropriate motor program
(patient may complete actions in incorrect order eg putting on shoes before socks); also loss of
ability to voluntarily perform a learned task when given necessary tools (eg try to comb hair with
toothbrush)
136. How do you differentiate between the vestibular nystagmus and the
congenital nystagmus?
-vestibular nystagmus: horizontal rotary, horizontal in different directions of gaze, amplitude
increases when eyes move in direction of fast phase
-congenital- inherited. Appears in childhood, horizontal jerk type, absent in sleep, variable visual
impariment, binocular
137. How do you treat a patient with acute malignant neuroleptic syndrome?
-cessation of offending neuroleptic pharmacologic agent
-supprotive therapy: hydration and treat hyperthermia with cooling blankets and ice packs
-bicarbonate might be beneficial to prevent renal failure
-bromocriptine mesylate (dopamine agonist) and dantrolene sodium (mm relaxant-inhibits Ca2+
release for SR)
138. What are the differences between tardive dyskinesia and levodopa-
induced dyskinesia?
- Levodopa-induced dyskinesia is a form of dyskinesia associated with levodopa, used to treat
Parkinson's disease. It often involves hyperkinetic movements, including chorea, dystonia, and
athetosis. In the context of Parkinson's disease (PD), dyskinesia is often the result of long-term
dopamine therapy
-tardive dyskinesia- side effect of antipsychotic medications. These drugs are used to treat
schizophrenia and other mental health disorders. TD causes stiff, jerky movements of your face
and body that you can't control.
141. What is the difference between neuropathic pain and nociceptive pain?
142. What are the clinical features alowing to differentiate between cerebella
tremor and a parkinsonian tremor?
Cerebellar tremor: intention tremor- slow, zig-zag mation when pointing, extending towards
target; ipsilateral to side of lesion
Parkinson tremor: resting tremor: uncontrolled movement of distal appendages (most noticeable
in hands); tremor alleviated by intentional movement (“pill rolling tremor”)
143. Describe the indirect cortico-strio-thalamo-cortical circuit for the control
of voluntary adaptive motor behavior
144. What is the clinical-evolution difference between the relapsing-remitting
and secondary-progressive forms of multiple sclerossi?
-Most people with multiple sclerosis -- around 85% -- have this type. They usually have their first
signs of the disease in their early 20s. After that, they have attacks of symptoms (called relapses)
from time to time, followed by weeks, months, or years of recovery (called remissions).
The nerves that are affected, how severe attacks are, the degree of recovery, and the time between
relapses all vary widely from person to person.
Eventually, most people with relapsing-remitting MS will move on to a secondary progressive phase
of MS.
-After living with relapsing-remitting MS for many years, most people will get secondary
progressive MS. In this type, symptoms begin a steady march without relapses or remissions. (In this
way, it’s like primary progressive MS.) The change typically happens between 10 and 20 years after
you’re diagnosed with relapsing-remitting MS.
It's unclear why the disease makes the shift. But scientists know a few things about the process:
The older a person is when she’s first diagnosed, the shorter the time she has before the
disease becomes secondary progressive.
People who don’t fully recover from relapses generally move to secondary progressive MS
sooner than those who do.
The process of ongoing nerve damage changes. After the transformation, there's
less inflammation and more of a slow decline in how well the nerves work.
Secondary progressive MS is tough to treat, and the disease can be hard to handle day to day.
Symptoms get worse at a different rate for each person. Treatments work moderately well, but most
people will have some trouble using their body like they used to.
145. What are the possible anatomic locations (at least 2) of a lesion which
clinically manifest as an ataxic hemiparesis (ataxia is present at the level of a
paretic limbs)?
Striatum, internal capsule
Type 1:wedge compression fracture with “tear drop” chip broken off anterior tip of vertebral
body.
Type 2: fracture of entire upper half of vertebral body with large segment broken free anteriorly.
Type 3: fracture through entire vertebral body with fragmentation of its anterior portion.
Type 4: “burst” fracture . entire vertebral body crushed with intraspinal bone fragments.
157. Describe the clinical features of the typical brown sequard syndrome.
also known as Brown-Séquard's hemiplegia is caused by damage to one half of the spinal cord,
resulting in paralysis and loss of proprioception on the same (or ipsilateral) side as the injury or
lesion, and loss of pain and temperature sensation on the opposite (or contralateral) side as the
lesion
Secondary tumors of the brain are metastatic and have invaded the brain from cancers originating
in other organs. Secondary brain tumors are more common than primary ones. primary tumor is
one that has started in the brain.
26 ) A brain tumor occurs when abnormal cells form within the brain.[2] There are two main types
of tumors: malignant or canceroustumors and benign tumors.[2] Cancerous tumors can be divided
into primary tumors that start within the brain, and secondarytumors that have spread from
somewhere else, known as brain metastasis tumors.[1] All types of brain tumors may produce
symptoms that vary depending on the part of the brain involved.[2] These symptoms may
include headaches, seizures, problem with vision, vomiting, and mental changes.[1][7][2] The
headache is classically worse in the morning and goes away with vomiting.[2] More specific
problems may include difficulty in walking, speaking, and with sensation.[1][3] As the disease
progresses unconsciousness may occur.[3]
159. What are the four main domains you must examine for language
evalution?
weakness, paralysis, or a lack of coordination of the motor-speech system, producing dysarthria.
160. What is the direction of the tonic component of the ocular nystagmus in a
patient with peripheral vestibular syndrome?
lesioned peripheral ves7bular complex may be less actvive ( hypovalent ) or abnormal
excessively ac1ve ( hypervalent – e.g. Meniere’s disease ); the tonic devia1on is always towards
the HYPOVALENT one.
163. What is the idiopathic trigeminal neuralgia and how do you treat it?
- mean age of onset is 52-58 years
- Tic Douloureux=paroxysms of intense, stabbing pain
- in the distribution of the mandibular and maxilary divisions
- the pain seldom lasts more than a few seconds and recur
frequently
- is so intense that the patient involuntarly winces
- initiated by stimulation of certain areas of the face, lips or
gums as in shaving or brushing the teeth or by chewing, talking or yawning=trigger zones
- the clinical exam is normal
- the mechanism of paroxismal pain is in the nature of allodynia
Treatment of TN comprises the following:
• Pharmacologic therapy
• Percutaneous procedures (eg, percutaneous retrogasserian glycerolrhizotomy)
• Surgery (eg, microvascular decompression)
• Radiation therapy (ie, gamma knife surgery
167. Name at least three different types of the localalization of a lesion (either
in the nervous or muscular system ) that would result in the absence of tendon
reflexes
Lower motor neuron lesions : Brachial plexus involvement : loss tendon reflexes affected upper
limb unilateral.
Femoral nerve injury : origin L2 ,3 ,4 roots .. knee tendonreflex abolished
Tibial nerve injury : sciatic nerve terminal division ..loss of achilean tendon reflex
173. What are the cardinal clinical findings in amyotrophic lateral sclerosis
(ALS)? Name at least 3 other diseases they may be part of the differential
diagnosis in the case of a patient with clinical findings suggestive for ALS
syndrome.
The triad:
1)atrophic weakness of the hands, arms or legs
2)generalized hyperreflexia
3)Coarse fasciculation evident in weakened muscles.
• Absence of sensory changes
• Normal sphincteric control
differential diagnosis:
1)Other Motor Neuron Diseases
▫ Primary lateral sclerosis
▫ Progressive muscular atrophy
Progressive bulbar palsy
•2) Neuropathies
▫ GB, CIDP
• 3)Myopathies
▫ Polymyosistis, inclusion body myositis
• 4)NM Junction
▫ Myasthenia gravis
• 5)Chronic compression of cervical
spinal cord
▫ Cervical disc protrusion
▫ Other causes of cervical mielopathy
6)Neurodegenerative Diseases
▫ Parkinson’s, Progressive Supranuclear
Palsy, MS
• 7)Malignancy
▫ Primary/mets CNS
▫ Motor neuron syndromes with multiple
myeloma, lymphoma, lung or breast
cancer
• 8)Toxic Exposure
▫ heavy metals
• 9)Endocrine
▫ TSH, adrenal, pituitary
• 10)Infectious
▫ HIV, CMV
174. For a patient with a mild clinical stage of Parkinson disease, are falls
frequent occurences or rather rare?
Stage One
1. Signs and symptoms on one side only
2. Symptoms mild
3. Symptoms inconvenient but not
disabling
4. Usually presents with tremor of one limb
5. Friends have noticed changes in posture, locomotion and facial expression
- so falls are rare. Stage one is the mild stage.
17) Name at least two types of involuntary movements that may be associated
with wilson’s disease.
175. Ischemic of anterior cerebral artery?
Occlusion of theA1 segment–
Usually well tolerated due to the collateral blood flow from the opposite hemisphere through the
ACoA
BilateralACAocclusion–paraplegia,incontinence,abulia,nonfluent aphasia,frontal lobe
personality disorder
Occlusion of the A2 segment
Sensory and motor deficit in the contralateral foot and (to a lesser extent) shoulder and hand,
with sparing of the face;
The motor deficit is more pronounced in the distal part of the lower limb
Eyes and head may be deviated to the side of the lesion
Patient may have urinary incontinence and contralateral grasping;
Speech disorders may appear–especially transcorticalmotor aphasia
Occlusion of the penetrating branches –the anterior limb of the internal capsule and caudate
nucleus are affected
176. What are the main cerebral lesions in the tuberous sclerosis complex.
BRAIN LESIONS
1. Cortical tuber (glioneuronal hamartomas)
2. White matter heterotopia (dysplastic/dysmyelinated lesions)
3. Subependymal nodules
4. Subependymal giant cell astrocytomas
182. Define schizencephaly, name the main causes and describe its clinical
aspect:
is a rare birth defectcharacterized by abnormal clefts lined with grey matter that form
the ependyma of the cerebral ventricles to the pia mater. These clefts can occur bilaterally or
unilaterally. Common clinical features of this malformation include epilepsy, motor deficits, and
psychomotor retardation.
In schizencephaly, the neurons border the edge of the cleft, implying a very early disruption of
the usual grey matter migration during embryogenesis. The cause of the disruption is not known,
but likely the cause may be either genetic or a physical insult, such as infection, infarction,
hemorrhage, in utero stroke, exposure to a toxin, or mutation
183. Name the conditons that have a potential neurosurgical management and
may result in clinical picture of pseudodementia syndrome
186. What are the clinical and paraclinical criteria necessary for the diagnosis
of cerebral death?
188. What are the criteria for positive diagnosis for type I spinal amiotrophy
( werdnig Hoffman disease?
189. What is the clinical difference between a vegetative state and minimally
conscious state ?