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1.

Motor homunculus-- descending motor pathways (projection)


o Picture representation of the(both):
 primary motor cortex(portion of the human brain responsible for
the processing and integration of motor information)
 primary somatosensory cortex (portion of the human brain
responsible for the processing and integration of tactile information).
o concept of "the body within the brain"
o the amount of cerebral tissue or cortex devoted to a given body region is
proportional to how richly innervated that region is, not to its size
o resembles an upside-down sensory or motor map of the contralateral side of the
body.
 upper extremities such as the facial body parts and hands are closer
to thelateral sulcus than lower extremities such as the leg and toes
o decussation in the pathways also result in right gyri to receive input from the left
side of the body and vice versa

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

3. Tendon reflex activity and muscle tone control


o Controlled by
 Large (alpha) motor neurons
 Muscle spindles
 Afferent fibers of the muscle spindles
 Small anterior horn cell (gamma) motor neurons- axons are
connected with the spindles

4. Difference btw LMN & UMN signs


o UMN
 Motor deficit extended to half of body or more group of muscles
 Spastic hypertonia
 Polykinetic reflexes
 Pathologic reflexes
 No abdominal cutaneous reflexes
 Absent atrophy or fasciculation
o LMN
 One isolated muscle or separate group of muscles
 Hypotonia in affected area
 Abolished reflexes or diminished
 Absent pathologic reflexes
 Atrophy of affected territory
 Fasciculations

5. Manifestations of complete transverse spinal cord section at T8 level


o Complete Spinal Cord Transection Syndrome check crash course
 •Upper motor neuron syndrome below the lesion
 •Initially – stage of spinal shock, hypotonia
 •Later – stage of severe spasticity
 •Anesthesia for all sensory modalities below the lesion (tactile,
temperature and pain anesthesia, reveals the lesion level, corresponding to
the affected dermatomes)
 •Trophic changes, pressure sores
 •There may be a narrow area of hyperesthesia at the upper edge of
the anesthetic zone
 •Upper motor neuron lesion in anterior horn can cause a deficit in
the brachial or lumbar plexus territory
 •Disturbances of sphincter control, with a loss of bladder and
bowel control
o Total motor deficit beneath the lesion
 Paraplegia for thoracic lesions
 Tetraplegia for cervical lesions
o Abolished voluntary control in:
 Urinary continence = incontinence
 Rectal continence = constipation
o Abolished sensitivity below this lesion

6. What lesion can cause muscle fasciculations


o Synonymous with muscle twitch
o Small local involuntary muscle contractin and relaxation which may be visible
under the skin
o Arise as a result of spontaneous depolarization of a lower motor neuron leading to
the synchronous contraction of all the skeletal muscle fibers within a single motor
unit

7. What lesion causes hemiballismus


o Large-amplitude, flinging hemichorea (affects proximal muscles) contralateral to
a vascular lesion of the subthalamic nucleus (often elderly diabetics). Recovers
spontaneously over months
o Lesion is found in subthalamic nucleus of Luys (most frequently of vascular
origin)
o The lesion can also be found in the globus pallidus or in its fibers and subthalamic
nucleus
8. Manifestations of Anton-Babinski syndrome
o visual anosognosia
o rare symptom of brain damage occurring in the occipital lobe
o sudden development of bilateral occipital dysfunction

9. Wernicke’s aphasia clinical features


o Impairment of comprehension of speech
o Relatively fluent but paraphasic speech. Incomprehensible when extreme
o Lesion involving the posterior one third of the superior temporal gyrus- near the
primary auditory cortex

10. Differentiate aphasia from anarthria


o Pure dysarthria or anarthria
o Theres no abnormality of the cortical language mechanism
o Pt. understands what is heard. No difficulty in writing and reading. Unable to utter
a single intelligible word
o When dominant frontal operculum is damaged

11. Difference btw generalized and focal features


o Generalized seizures
 Abrupt initial loss of consciousness
 Generalized tonic clonic seizures
 Absence seizures
 Myoclonic seizures
 Atonic seizures(one of the most severe type, onset only during
childhood, hallmark of intractable, deteriorating epilepsies like lennox
gastaut syndrome)
o Focal (partial) seizures
 Consciousness retained, patient able to describe the clinical content
of his seizures
 Simple focal seizures
1. Consciousness retained during the whole episode
2. Seizure focus located in a cortical zone responsible for highly
complex, integrative functions  usually temporal or frontal lobes
or propagation of seizures into such complex cortical territories
(hippocampal structures, orbitofrontal cortex etc.)
3. Simple or complex focal seizures with secondary tonic-clonic
generalization

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

15. Describe pyramidal spasticity and parkinsonian rigidity


o They are both types of hypertonia
o Extrapyramidal rigidity
 Diffuse increase in muscle tone to passive movement that occurs
primarily with lesions that involve the basal ganglia
 Increased tone
 Both flexor and extensor muscles are involved with resistance to
passive movement in all directions
 Increased tone is equally present from beginning to end of
movement and doesn’t vary with speed of movement
1. This type of rigitidy is refered to as lead pipe
 Involved muscles may be firm and tense to palpation
 After being placed in a new position, the part may remain there,
causing the limbs to assume awkward postures (plasticity or waxy
flexibility
o Spasticity
 Due to lesions involving the corticospinal pathways
 Differs from rigidity because its not uniform throughout the range
of movement, and it varies with the speed of movement
 Rigidity tends to affect all muscles to same degree, but spasticity
varies from muscle to muscle
 If passive movement is made slow, then there may be little
resistance
 If passive movement is made quickly, then theres a sudden
increase in tone partway through the arc, causing a block as though the
muscle had impacted a stop
 Increase in muscle tone is more marked in the flexor and pronator
muscles of the upper limb and the extensors and internal rotators of the
lower limb
 Passive motion may be carried out with little difficulty if done
through a small range of movement, but resistance increases if an attempt
is made to move the extremities through a greater range
 Slow passive movement may be carried out with relative ease, but
on rapid movement, there is blocking or catching often with a waxing
followed by a sudden waning of tone at the extremes of the range of
motion (clasp-knife phenomenon)

16. Features of Parkinson tremor


o The classic “resting tremor” of Parkinson's disease has characteristic clinical
features. The tremor has a frequency of 4 to 6 cycles per second, typically with a
“pill rolling” character when it involves the hand. It is generally present with the
limb in complete repose and typically subsides when the limb moves and takes up
a new position, although the tremor may reemerge (“reemergent tremor”) within a
short time after maintaining the new position. Because resting tremor diminishes
or subsides with action, it may not be disabling but can be embarrassing and may
be associated with aching or fatigue of the affected limb. Resting tremor is usually
accentuated by stress (e.g., by asking the patient to perform mental calculations).
It is also characteristically present in the upper limbs while walking. A higher-
frequency (e.g., 7 to 10 Hz) postural and kinetic tremor is also common in
patients with various causes of parkinsonism.

17. Manifestations of supranuclear palsy


o Initial symptoms
 2/3 of cases
1. Loss of balance
2. Lunging forward when mobilizing
3. Fast walking
4. Bumping into objects or people
5. Falls
o Later symptoms
 Dementia
 Sluring of speech
 Difficulty swallowing
 Difficulty moving the eyes particularly in vertical direction
o Cardinal manifestations:
 Supranuclear ophthalmoplegia
 Neck dystonia
 Parkinsonism
 Pseudobulbar palsy
 Behavioral and Cognitive impairment
 Imbalance and Difficulties walking
 Frequent falls

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

19. Diffuse Lewy body disease


o Dementia preceding motor signs
 Visual hallucinations
 Episodes of reduced responsiveness
o if parkinsonism has been present for 12 months or longer before cognitive
impairment is detected, the disorder is called Parkinson disease with dementia;
otherwise, it is called DLB
o orthostatic hypotension appears to be particularly common in patients with DLB,
even when dementia is mild

20. Classes of anti-parkinsonian drugs


o Dopaminergic
 Levodopa
 Dopamine agonists
1. Ergot
2. Non ergot
 Selective MAO-B inhibitors
o Non dopaminergic
 Anticholinergic agents
1. Trihexyphenidyl
2. Benztropine
 NMDA antagonists
1. Amantadine

21. Drug of choice for psychosis in Parkinson


o Clozapine?
o It is possibly drug-induced

22. Motor fluctuations in Parkinson, description and cause


o apomorphine is available for subcutaneous injections and may be useful in
patients with levodopa-related motor fluctuations
o Motor fluctuations are the oscillations, or variations, in the control of motor
symptoms associated with the long term use of the medication, levodopa.
 Levodopa induced motor complications consists of fluctuations in
motor response and involuntary movements known as dyskinesias

23. Side effects of levodopa treatment


o reduced response to L-dopa and to paradoxical and excessive movements
(dyskinesias)
o Development of motor and nonmotor fluctuations
o Occurrence of nonmotor dopaminergic adverse effects (less frequently than with
other drugs): nausea, neuropsychiatric problems including hallucinosis,
sleepiness, autonomic problems
o Nausea, vomiting, orthostatic hypotension avoided by gradual titration

24. Tardive dyskinesia, definition & causes


o Incurable and difficult to treat disorder resulting in involuntary, repetitive body
movements
o Involuntary movements are tardive (slow or belated onset)
o Clinical features
 Abnormal choreoathetoid movements
1. adults
a. Face and mouth
i. Blepharospasm
ii. Torticollis
iii. Oromandibular dystonia
2. Children
a. limbs
o Causes
 Long-term or high dose antipsychotic drugs due to dopamine
receptor antagonism
 Higher risk with advancing age
 When medication is withdrawn relatieley early the dyskinesia may
reverse
 After 6 months of exposure the movement disorder may persist
indefinitely
 Drugs
1. Dopamine antagonists
a. Haloperidol, metoclopramide
2. Antiepileptics
a. Phenytoin, carbamazepine, valproic acid, felbamate
3. Dopamine agonists
a. Levodopa
4. MAOIs
5. Adrenergic agents
a. Amphetamines, methylphenidate, caffeine
6. Beta agonists
a. Antihistamines
7. TCAs
a. Busipirone, lithium
8. Cimetidine
9. oral contraceptives
 Cocaine

25. Evolution of Huntington and main


26. causes
o Dementia and the psychiatric features of HD are perhaps the earliest and most
important indicators of functional impairment.
o dementia syndrome associated with HD includes early onset behavioral changes,
such as irritability, untidiness, and loss of interest.
 slowing of cognition, impairment of intellectual function,and
memory disturbances are seen later.
o Early stages of HD are characterized by deficits in short-term memory, followed
by motor dysfunction and a variety of cognitive changes in the intermediate stages
of dementia.[6, 7] These deficits include diminished verbal fluency, problems
with attention, executive function, visuospatial processing, and abstract reasoning.
Language skills become affected in the final stages of the illness, resulting in a
marked word-retrieval deficit.
o Initially, mild chorea may pass for fidgetiness. Severe chorea may appear as
uncontrollable flailing of the extremities (ballism) which interferes with function
o As the disease progresses, chorea coexists with and gradually is replaced by
dystonia and parkinsonian features, such as bradykinesia, rigidity and postural
instability, which are usually more disabling than the choreic syndrome per se
o In advanced disease, patients develop an akinetic-rigid syndrome, with minimal or
no chorea
o Other late features are spasticity, clonus, and extensor plantar responses
o Main cause of death:
 Pneumonia (largest risk)
 Heart disease
 Suicide

27. Criteria for Wilson diagnosis


o combination of serum ceruloplasmin level, urinary copper excretion, presence of
Kayser-Fleischer rings, and hepatic copper content when biopsy is required.
o The presence of Kayser-Fleischer rings and ceruloplasmin levels of less than 20
mg/dL in a patient with neurologic signs or symptoms suggest a diagnosis of
Wilson disease.
o If asymptomaticliver biopsy for quantitative copper determination is essential
to establish the diagnosis of Wilson disease.
o Genetic testing is limited to screening of family members for an identified
mutation detected in the index patient
o Brain imaging shows characteristic findings; MRI appears to be more sensitive
than CT in detecting early lesions
 characteristic "face of the giant panda" sign has been described,
formed by high signal intensity in the tegmentum (except for the red
nucleus), preserved signal intensity of the lateral portion of the pars
reticulata of the substantia nigra, and hypointensity of the superior
colliculus
o Serum Ceruloplasmin
 levels are low in newborns and gradually rise within the first 2
years of life
 90% of all patients with Wilson disease have ceruloplasmin levels
of less than 20 mg/dL(reference range, 20-40 mg/dL)
 Ceruloplasmin is an acute phase reactant and may be increased in
response to hepatic inflammation, pregnancy, estrogen use, or infection
 Falsely low ceruloplasmin levels may be observed in any protein
deficiency state, including nephrotic syndrome, malabsorption, protein-
losing enteropathy, and malnutrition
 Ceruloplasmin levels may also be decreased in 10-20% of Wilson
Disease gene heterozygotes, who do not develop Wilson disease and do
not require treatment
o Urinary and hepatic copper excretion
 Urinary
1. greater than 100 mcg/d (reference range, < 40 mcg/d) in most
patients with symptomatic Wilson disease
2. rate may also be elevated in other cholestatic liver diseases.
 Hepatic
1. criterion standard for diagnosis of Wilson disease
2. liver biopsy with sufficient tissue reveals levels of more than 250
mcg/g of dry weight even in asymptomatic patients

28. Treatment of Wilson’s disease


o lifelong use of chelating agents (eg, penicillamine, trientine)
o Surgical decompression or transjugular intrahepatic shunting (TIPS) is reserved
for recurrent or uncontrolled variceal bleeding unresponsive to standard
conservative measures
o Orthotopic liver transplantation is curative
o Other:
 Anticholinergics, baclofen, GABA antagonists, and levodopa to
treat parkinsonism and dystonia
 Antiepileptics to treat seizures
 Neuroleptics to treat psychiatric symptoms
 Protein restriction, lactulose, or both to treat hepatic
encephalopathy

29. Treatment of Sydenham chorea


o Includes antibiotic, neuroleptic, and cardiac medications
 Penicillin
 Oral cephalosporin if allergic to penicillin
o Anticonvulsants
 Valproic acid and carbamazepine
o Dopaminergic blockers
 Pimozide and haloperidol
o Neuroleptics
 Haloperidol and pimozide
o Steroids
 Prednisone if patient has carditis
 Decreases myocardial inflammation

30. Cervical dystonia, clinical types


o Rotational torticollis
 Causes head to twist
o Retrocollis
 Extends
o Anterocollis
 Flexes
o Laterocolis
 Tilts towards the shoulder

31. Management of dystonias


o Rehabilitative therapies
o Oral medication
o Neurochemolytic interventions
o Surgery

32. Definition of transient ischemic attack


o imagistic studies (MRI) doesnt show a lesion of the brain
o duration of the symptoms ≤ 24 h, but typical TIAs last ≤ 1
o The important distinction between a transient ischemic attack (TIA) and a stroke
is whether the ischemia has caused brain infarction, a difference that may not be
possible to distinguish within the first few hours after the onset of symptoms but
commonly becomes apparent retrospectively. With a stroke, symptoms usually
persist for more than 24 hours, but clinical deficits that persist for more that 1 to 2
hours commonly are associated with permanent brain damage, often demonstrable
by computed tomography (CT) or magnetic resonance imaging (MRI), despite
complete recovery. Many events that were defined as TIAs in the era before
neuroimaging were actually infarcts.By comparison, the symptoms of TIAs
usually do not persist for more than 1 to 2 hours and do not cause permanent
damage on neuroimaging studies. Patients with TIAs are at considerably increased
risk of having a stroke within hours to days after a TIA.
o Blood flow is restored and no infarct occurs
33. Therapeutic window for fibronolysis in ischemic stroke
o IV rtPA (recombinant plasminogen activator)
 Within 3 hours from onset of symptoms

34. Treatment and secondary prevention of ischemic stroke in atrial


fibrillation
o Anticoagulant therapy warfarin
o Risk reduction with treatment
 68% warfarin
 21% aspirin

35. Perfusion-diffusion mismatch & importance in acute stroke


treatment
o Diffusion weighted imaging(DWI) and perfusion weighted imaging(PWI) are
checked in an MRI
o DWI
 Reflects biochemical compromise (core of infarction)
 Changes are visible within the first hour after the vessel
obstruction (in 3 hours 100% of patients will show hanges on DWI
sequences)
o PWI
 Reflects hemodynamic compromise
 Differences between the 2 areas represents the salvageable tissue
(penumbra)
o Its important because it shows the penumbra, measures should be taken to
restore blood flow to avoid infarction of penumbra
 Measures= revascularization

36. 5 causes of cardio-embolic stroke


o Arrhythmias
 Atrial fibrillation (most common)
o Mural thrombi
 Dyskinetic myocardium, cardiomyopathy
o Valvular heart disease
 Rheumatic heart disease, endocarditis
o Paradoxical emboli
 Patent foramen ovale, atrial septal defect, arteriovenous
malformation

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

38. Clinical feature of infarction in cortex supplied by left ACA


o Both arteries are connected with anterior communicating artery so the occlusion
depends on the relation to the anterior communicating artery
 Proximal occlusion to the ant. Comunicating artery
1. Normally well tolerated because of adequate cross flow so fewer
symptoms
 Occlusion distal from anterior communicating artery
1. Contralateral weakness and cortical sensory loss in the leg
2. Incontinenc
3. Contralateral grasp
4. Other primitive reflexes
o Sensory and motor deficit in the contralateral foot and (to a lesser extent) shoulder
and hand, with sparing of the face
o The motor deficit is more pronounced in the distal part of the lower limb
o Eyes and head may be deviated to the side of the lesion
o Patient may have urinary incontinence and contralateral grasping;
o Speech disorders may appear– especially transcortical motor aphasia

39. Clinical features of ischemic stroke in superficial territory of left


MCA distribution
o Superficial = m2 segment
o Superior trunk
 Contralateral sensory and motor deficit of the face and upper limb
and to a lesser degree, of the lower limb
 Eyes and head are deviated to the side of the lesion
 It mimics the M1 occlusion (except the milder involvement of the
lower limb)
 Global aphasia initially– later it evolves into predominantly motor
aphasia
o Inferior trunk
 Predominantly expressive aphasia

40. Sensory deficiencies in Wallenberg syndrome + topographic


distribution
o PICA (posterior inferior cerebellar artery) Occlusion= Lateral Medullary
Syndrome =WALLENBERG SDR
o PICA is a branch of vertebral artery
o lateral medullary syndrome, consists of severe vertigo, nausea, vomiting,
nystagmus, ipsilateral ataxia (of the cerebellar type), and ipsilateral Horner’s
syndrome (ptosis, miosis, and decreased sweating)
 also includes ipsilateral loss of facial pain and temperature
sensation and contralateral loss of these sensory modalities in the trunk
and limb
o Occlusion=
 Ipsilateral loss of facial sensation
 Ataxia
 Contralateral hemiparesis
 Sensory loss

41. Secondary stroke prevention in pt with angioplasty with stent for


symptomatic carotid stenosis >75%
o Symptomatic stenosis >70% must be revascularized
 Best results if performed in 1st 14 days after stroke
 Patients with carotid stenting should receive for at least 30 days
after the procedure a combination of Clopidogrel 75 mg/day + Aspirin 75
mg/day

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

43. Main criteria for carotid endarterectomy


o In symptomatic good-risk patients with surgical morbidity and mortality (stroke
and death) of <6 %
 One or more TIA in preceding 6 months and carotid artery
stenosis >50%
o In a asymptomatic good risk patients treated by surgeons with surgical mortality
and morbidity of <3% indication for CEA is stenosis exceeding 60%
o If with complications from endovascular intervention when CA is >70% by
noninvasive imaging or >50% by catheter imaging
 Carotid angioplasty and stenting is indicated as an alternative to
CEA

44. Signs of subarachnoid hemorrhage


o symptoms
 Nuchal rigidity
 Headache often upon straining
 Central feature: sudden onset of severe headache  thunderclap
headache
1. May be accompanied by nausea and/or vomiting and meningeal
irritation(nuchal rigidity and pain, back pain, bilateral leg pain)
o Signs
 Mild to moderate BP elevation
 Hyperthermia secondary to chemical meningitis from subarachnoid
blood products
1. Common after 4th day following bleeding
 Tachy cardia
1. Several days after hemorrhage
 Papilledema on fundoscopy and retinal hemorrhage
 Cranial nerve palsies, along with memory loss, are present in 25%
of patients
1. most frequent is oculomotor nerve palsy with or without ipsilateral
mydriasis, which results from rupture of a posterior
communicating artery aneurysm
2. Abducens nerve palsy is usually due to increased ICP rather than a
true localizing sign
3. Monocular vision loss can be caused by an ophthalmic artery
aneurysm compressing the ipsilateral optic nerve.
 Hemiparesis results from middle cerebral artery (MCA) aneurysm,
ischemia or hypoperfusion in the vascular territory, or intracerebral clot.
Patients may also have aphasia, hemineglect, or both. Leg monoparesis or
paraparesis with or without akinetic mutism/abulia points to anterior
communicating aneurysm rupture.

45. Diagnose, prevent & treat vasospasm in pts with subarachnoid


hemorrhage
o delayed ischemia from arterial smooth muscle contraction of the large
capacitance vessels at the base of the brain is the leading cause of death and
disability following aneurysmal SAH
o Vasospasm is symptomatic in 36% of patients
o Risk factor for vasospasm
 Larger volumes of blood in subarachnoid space
 Clinically severe SAH
 Female sex
 Young age
 Smoking
o vasospasm typically has its onset on day 3 after SAH, is maximal at about days
6-8, and usually resolves around day 12
 clinical onset differs according to whether the patient has had a
prior SAH
o Imaging
 Conventional angiography
 Transcranial Doppler
 Ct
o For prevention
 Maintanence of normovolemia, normothermia and normal oxygen
 Oral nimodipine for prevention
 Thrombolytic therapy
1. Recombinant tissue plasminogen activator (rTPA) reduces risk of
vasospasm
 CSF drainage decreases incidence of vasospasm
 Statins  prevents vasospasm and delays cerebral ischemia
o Treatment
 Triple H therapy
1. Hypertension inotropes and vasopressors (dobutamine)
2. Hypervolemia packed erythrocytes, isotonic crystalloid, and
colloid and albumin infusions in conjunction with vasopressin
injections
3. Hemodilution(transfusion) to maintain hematocrit at 30-35%
 Transluminal balloon angioplasty
1. Recommended if failure of conventional therapy
2. not effective in direct treatment of vasospasm of more distal
vessels

46. 3 most common causes of cerebral hemorrhage in adults


o Trauma, chronic HTN, and cerebral amyloid angiopathy
o The most common nontraumatic causes : chronic hypertension; ruptured
intracranial aneurysms; vascular malformation(cerebral amyloid angiopathy)

47. Locations of cerebral hemorrhage caused by chronic HTN


o Hypertension is associated with hemorrhage in various locations throughout the
brain, especially in the external capsule–putamen, internal capsule–thalamus,
central pons, and cerebellum
-What are the most common sites for lesions characteristic for
cerebral small vessel disease in patients with chronic arterial
hypertension?
Small vessels (Basal ganglia, thalamus, pons,cerebellum) can cause
charcot-bouchard microaneurysm
o Putamen is most common site
o

48. Interventional treatment of intracranial aneurysms


o Objectives  exclude aneurysm from circulation or relieve pressure on
adjacent brain tissue caused by expansion of sack
o Percutaneous angiography
 electrical current applied to a detachable coil threaded into an
aneurysm causes surrounding blood to clot
 coil is detached and left in place, and the catheter is then removed.
o With very large aneurysms, for which use of a coil is not possible, wrapping
the sack with various types of material to prevent it from rupturing or
growing is sometimes performed
o Indirect procedures include various methods of occluding the feeding artery
49. Anatomy of brain venous circulation
o Superficial venous system
 Superior cerebral group
1. Drainage for Dorsolateral and dorsomedial surfaces of
hemisphere
2. Enter superior sagittal sinus
3. Most prominent  in central sulcus= superior anastomotic vein
of Trolard which interconnects superior and middle group of veins
 Middle cerebral group
1. Veins run along the sylvian fissure
2. Drain inferolateral surface of hemisphere
3. Open in cavernous sinus
 Inferior cerebral group
1. Drain inferior surface of hemisphere
2. Open into cavernous and transverse sinuses
3. Inferior anastomotic vein of Labbe interconnects the middle and
inferior groups
 Medial surface  drained by veins which open into superior and
inferior sagittal sinuses, and basal vein and great cerebral vein of galen
o Deep venous system
 2 main drainages: internal cerebral vein & basal vein of Rosenthal
1. These 2 join beneath splenium of corpus callosum to form the
great cerebral vein of Galen which opens into the straight sinus
2. There are many anastomotic interconnections
a. Only Great cerebral vein and basal vein of Rosenthal
Obstruction will affect deep venous flow

50. Cavernous sinus (or superior saggital sinus) venous thrombosis


manifestations
o Headache
o Increased intracranial pressure and papilledema
o Motor deficits (even bilateral deficits) and seizures are frequent
o With or without scalp edema and dilated scalp veins
o Presentation as isolated intracranial hypertension syndrome is infrequent
o Ocular signs
 Orbital pain
 Chemosis?
 Proptosis
 Oculomotor palsys
o Loss of sensibility on face (V1 and V2)
o Frequently septic due to nearby infections

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%

52. 5 causes/risk factors of cerebral venous thrombosis


o Risk factors
 Acquired risks
1.Surgery
2.Trauma
3.Pregnancy; puerperium
4.Antiphospholipid syndrome
5.Cancer
6.Exogenous hormones
 Genetic risks
1.Inheritied thrombophilia
 Most frequent:
i. Genetic and acquired prothrombotic states
ii. Pregnancy and puerperium
iii. Infections
o Causes (15% of cases no underlying cause can be identified)
53. Treatment of cerebral venous thrombosis
o Acute antithrombotic treatment Either IV unfractioned heparin, or
subcutaneous low molecular weight heparin
o Management and prevention of early complications
 Elevated intracranial pressure(icp) and herniationmannitol;
osmotic diuretics; hemicraniectomy
 Seizures 
o Antibiotics with/without surgical drainage of infectious sources
o Analgetic treatement for headache
o For women with CVT during pregnancy, LMWH in full anticoagulant doses
should be continued throughout pregnancy, and LMWH or vitamin K antagonist
with a target INR of 2.0 to 3.0 should be continued for at least 6 weeks
postpartum (for a total minimum duration of therapy of 6 months)
o
54. Manifestations of a migraine attack without aura
o at least 5 attacks fulfilling criteria B through D
o B) headache attack lasting 4-72 hours (untreated or successfully treated
o C) headache has at least 2 of the following characteristics
 unilateral location
 pulsating quality
 moderate or severe pain intensity
 aggravation by or causing avoidance of routine physical activity
o D) during headache at least one of the following
 nausea &/or vomiting
 photophobia and phonophobia
o E) not attributed to other disorder

55. Describe cluster headache


o Trigeminal autonomic cephalalgias, including cluster headaches, are unilateral
headaches associated with ipsilateral autonomic features
o Cluster headaches are almost always unilateral, rarely bilateral, and have
characteristic ipsilateral autonomic features, commonly including lacrimation and
conjunctival injection and sometimes including nasal congestion, rhinorrhea,
ptosis, miosis, flushing, and eyelid edema
o The location of the pain is usually behind or above the eye or in the temple, but
other areas of pain can include the forehead, cheek, teeth, or jaw
o The diagnostic criteria for cluster headache include severe unilateral orbital,
supraorbital, or temporal pain persisting for 15 to 180 minutes with at least one of
the following: ipsilateral conjunctival injection or lacrimation, nasal congestion or
rhinorrhea, eyelid edema, forehead and facial sweating, miosis with or without
ptosis, and restlessness or agitation. Attacks occur between once and as often as
eight times each day. There is no other cause of the disorder.

56. Direction of tonic deviation in a pt with peripheral vestibular


syndrome
o Peripheral vestibular syndrome
 Short duration
 Vertigo
 Objective:
1. Positive Romberg
2. Outstretched arm test part with lesion deviates
3. Horizontal nystagmus
o Related to the muscle groups where tonic deviation is present
 Extrinsic ocular muscles → VESTIBULAR NYSTAGMUS
1. direction: horizontal, vertical ( always central – mesencephalic ori
-gin )
2. Rotatory,retraction ( extremely rare, always central – mesencephali
origin)
 Upper limbs
1. Arm deviates to lesion side
 Axial (postural) muscles
1. Romberg never positive in cerebellar sdr.
a. Constant lateral deviation  vestibular
b. Variable random lateral deviation proprioceptive
c. Alternative systematic lateral deviation psychogenic,
malingering

57. Clinically isolated syndrome & treatment


o Clinically isolated syndrome (CIS) is a term that describes a first clinical episode
with features suggestive of multiple sclerosis (MS)
o Several studies indicate that treatment of patients with CIS with IFN-β1 delays
the onset of the defining second relapse and/or MRI defining lesion to meet the
criteria of MS as does a study of glatiramer acetate.
o Severity of deficit from the first attack, lesion load or volume, evidence of
atrophy or non-gadolinium-enhancing T1 hypointensities on initial or repeat MRI
in 3–6 months have all been suggested as guidelines to treat CIS patients with
DMT(disease modifying therapies).
 Natalizumab
 Glatiramer acetate (GA)
 IFN-B1
 neutralizing antibodies (NAbs)

58. Hypointense lesion on T1 MRI enhancing after contrast


administration –significance?/ T1 MRI in MS will explore what?
o A T1-weighted magnetic resonance imaging (MRI) scan shows “black holes,”
which are areas of permanent axonal damage. These are called hypointense
lesions, meaning that they display as dark areas on the MRI image. T1-weighted
lesions can also be areas of edema (swelling), which are not permanent and
disappear on subsequent scans.
o The T1-weighted scan is part of conventional MRI technology which is used to
monitor and diagnose multiple sclerosis (MS), usually in conjunction with a T2-
weighted scan and with gadolinium enhancement also known as : hypointense
lesions, “black holes”

59. Treatment for MS relapse


o Many relapse symptoms can be treated with high-dose corticosteroids, usually Solu-
Medrol
o The steroid treatment usually significantly shortens the duration of the most severe
symptoms, allowing a faster return to normal activities
o There is no cure for MS, but several drugs have been approved in the United
States as long-term maintenance therapy to reduce the rate of attacks in relapsing-
remitting MS: beta-interferon, glatiramer acetate, and natalizumab. These drugs
are indicated for relapsing-remitting disease or clinically isolated syndromes and
are probably useless for the progressive,degenerative aspects of MS

60. 5 protective factors for Alzheimer’s


o genetics
o education
o lifestyle diet, excercise
o pharmacological intervention statine; antiHTA; anti inflammatory drugs;
nsaids; antioxidants
o prevention of cerebrovascular accident

61. Clinical signs of Alzheimer’s


o Early symptoms of AD include forgetfulness for recent events or newly acquired
information, often causing the patient to repeat himself or herself. Other early
features are disorientation, especially to time, and difficulty with complex
cognitive functions such as mathematical calculations or organization of activities
that require several step

62. Microscopic hallmark of Alzheimer’s


o Amyloid deposition
 Diffuse plaques in elderly
 Compact plaquesassociated with neuritic changes caused by
toxic effects to dentdrites and axons
 Cerebral amyloid angiopathy:
a. Amyloid deposits in blood vessels inc risk for
hemorrhage
o Global loss of neurons

63. Mild cognitive impairment (criteria)


o 1) concern regarding a change in cognition
 In comparison to the persons prior level
o 2) impairment in one or more cognitive domains
 Lower performance in one or moreo cognitive domains that is
greater than would be expected for the patients age and educational
background
o 3) preservation of independence in functional abilities
 Mild problems performing complex functional tasks
 Generally maintain their independence of function in daily life
o 4) not demented

64. Main subtypes of vascular dementia


o Multiple large infarctions, which usually involve cortical and subcortical tissue
o Single or multiple smaller infarctions that involve critical brain regions

65. Diagnose and treat cerebral abscess


o Diagnosis
 Ct and mri
1. Ct capsule of the abscess enhances and the center of the abscess
and the surrounding edematous white matter are hypodense
2. Mri
a. T1:capsule enhances and the interior is hypointense
b. T2: the surrounding edema is apparent and the capsule is
hypointense
c. Cerebritis appears as dot-sized areas of deceased density
that enhance with gandolinum
 CSF exam
1. In the early stages mild to moderate pleocytosis with 10-80%
neutrophils
2. The protein content is modestly elevated
3. Glucose values not lowered
4. Csf is sterile, unless there is concomitant bacterial meningitis
 Blood cultures
 Sedimentation rate
 Chest x-ray
 ecocardiography
o Treatment
 Early: IV antibiotics penicillin G or third generation
cephalosporin and either chlomramphenicol or metronidazole
 Raised ICP (intracranial pressure) aspirate abscess or remove by
open procedure
 If abscess is solitary, superficial and well encapsulated  total
excision
 If abscess is deep stereotactical aspiration (method of choice)

66. Most probable Dx in a pt with infection who suddenly develops


paraparesis
o Paraparesis is weakness affecting both lower extremities
o Transverse myelitis

67. Herpes encephalitis


o Herpes simplex encephalitis (HSE) is an acute or subacute illness that causes both
general and focal signs of cerebral dysfunction
o Swelling and herniation of the temporal lobes through the tentorial opening may
occur, leading to coma during the first few days of the illness
o lesions take form of intense hemorrhagic necrosis of the inferior and medial
temporal lobes and the medioorbital parts of the frontal lobes
o The temporal lobe lesions are usually bilateral but not symmetrical
o Fever, headache, seizures, confusion, stupor, coma

68. Differential diagnosis for ALS


o Other conditions that may affect the pyramidal tract and lower motor neurons
or mimic some of their clinical features include cervical cord/foramen magnum
lesions (tumor, syringomyelia, syringobulbia, spondylosis), thyrotoxicosis,
hyperparathyroidism, dysproteinemia, paraneoplastic conditions, and
hexosaminidase A deficiency.

69. 2 variants of Guillain-Barre


o Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) due to an
immune attack on Schwann cell membrane or myelin sheath.
o .Acute (motor or motor-sensory) axonal neuropathy (AMAN or AMSAN) due to
an immune attack against the axolemma/axoplasm. This presentation is
distinguished from severe cases of AIDP, in which secondary axonal damage may
occur. AMAN is much more common in Asia and occurs mainly in children.
AMSAM may occur anywhere and affects adults preferentially. AMSAM has a
much worse prognosis than AMAN, with only 20% of patients with the former
ambulating at 1 year.

70. Treatment of Guillain-Barre


o PE (plasma exchange) and IV immunoglobulin within 2 weeks of the illness
equally improve the degree and rate of recovery
o Corticosteroids not indicated

71. Clinical manifestations and 3 causes of syringomyelia dissociation


o Loss of pain and temperature sense; impairment of thermoalgesic sensation, with
intact deep sensory function
o Due to: lesion in region of central canal of spinal cord implicating spinothalamic
fibers with preservation of other sensory modalities
o It can be associated with segmental amyotrophies, abolition of OTR (impairment
of anterior horn)
o Sensory modifications appear as hypoesthesia regions, corresponding to the
affected segment Initially described in syringomyelia, it can occur in
intramedullary tumors , trauma or hemorrhage
o 3 causes
 Wallenberg syndrome
 Brown sequard hemisection
 Complete transection

72. Muscles innervated by CN III + clinical effect of their paresis


o Levator palpebrae superior  partial ptosis
o opthalmoplegia
 Superior rectus
 Inferior rectus
 Medial rectus
 Inferior oblique

73. Differentiate peripheral from central CN VII paresis


o Peripheral = upper and lower ipsilateral; facial nucleus lesion
o Central = lower half of face, opposite site of lesion
 Due to central motor lesion

74. Diagnosis of myopathy


o Blood tests
 cK
 aldolase
 transaminases
 electrolytes: sodium, potassium, chloride
 thyroid check up
 autoimmune
 toxicology
 serology for viral or parasitic infections
o Electrophysiology
 Nerve conduction studies are normal
 Needle electrode test of muscular activity at rest and gradual to
maximal contraction
 At rest
1. Fibrillation potentials
a. Markers for spontaneous contractions of individual muscle
fibers as a consequence of membrane instability- very
prominent in inflammatory myopathies during the active
episodes
2. Myotonic discharge
a. Repetitive high frequency potentials expression of delayed
muscle relaxation after voluntary contraction
o Imaging studies
 Ct scan, mri or ultrasound
1. Pattern of involvement
2. Inflame, edema, musc mass
3. Normal appearance of thigh muscles
o Biopsy
o Genetic tests
o Assess cardiac function for associated cardiomyopathy

75. 5 causes of symmetric coma


o Traumatic damage
o Bilateral infarcts
o Hemorrhages
o Encephalitis
o Hypoxia

76. Causes of coma associated with meningeal syndrome (meningismus)-


slide 14 in coma
o Disease that cause meningeal irritation with or without fever, with an excess of
WBCs or RBCs in the CSF usually without focal or lateralizing cerebral or
brainstem signs
 Subarachnoid hemorrhage from rupture aneurysm arteriovenous
malformation, occasionally trauma
 Acute bacterial meningitis
 Some forms of viral encephalitis

77. Drug of choice for psychotic manifestations of Parkinson's, describe


why?
o Clozapine for hallucinations
o May be caused by levodopa

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

79. Microscopic pathological hallmark of Alzheimer's disease?


o Amyloid plaques and neurofibrillary tangles(tau protein)

80. The most likely location of a lesion to cause fasciculations in the


muscles.
o Lower motor neuron lesion

81. Describe the clinical aspect of complete paralysis of the common


oculomotor nerves.
o Sphincter pupillae dilated pupils
o down and out position
o outwards because the lateral rectus (innervated by the sixth cranial nerve)
maintains muscle tone in comparison to the paralyzed medial rectus
o downward, because the superior oblique (innervated by the fourth cranial or
trochlear nerve), is unantagonized by the paralyzed superior rectus, inferior
rectus and inferior oblique.
o the affected individual will also have a ptosis, or drooping of the eyelid,
and mydriasis (pupil dilation)

82. Which paraclinical exam is needed for MS diagnosis?


o MRI
o Evoked potentials

83. Carotid endarterectomy caused tongue paralysis. Explain.


o Injury to the hypoglossal nerve

84. Wallenberg syndrome clinical pictures


o

85. Epilepsy: general and focal differentiation


o General  abrupt initial loss of consciousness
o Focal consciousness is retained, patient is able to describe clinical content of
seizure

86. First manifestations of Alzheimer disease


o Memory loss
o Confusion
o Repetition

87. Stroke in the (L) MCA, describe the clinical picture


o Right hemiplegia
o Right gaze paralysis and homonymous hemianopsia
o Neglect of left perceptual space
o Aphasic

88. Aneurysm of the brain, treatment


o Embolization (coil embolization)
o Surgical clipping (at base of aneurysm)

89. CTS(carpel tunnel sdr.) describe the clinical picture


o Median nerve compression
o Pain at night

90. The main cause of intracranial bleeding


o Subarachnoid Berry aneurysm rupture (berry aneurysm most common at ant
communication artery and an cerebral artery in circle of willis)
o Primary intracerebral hemorage  chronic untreated hypertension
o Subdural and extradural hemorrhage rupture of cortical vein in elderly and
alcoholics and traumatic tear of middle meningeal artery respectively

91. 2nd prevention stroke due to ischemia


o Treat risk factors (ACEi+indapamide for atrial htn)
o Lifestyle changes
o Oral anticoagulants in cardioembolic stroke (esp in AF)(ex: warfarin in atrial
fibrilation)
o Antiplatelets (aspirin+ clopidogrel)
o Revascularization (symptomatic stenosis >70%) within 14 days after stroke

92. Describe the motor impairment of a patient with meningioma of falx


cerebri, which exerts compression on both medial aspects of frontal
lobes.
o Leg weakness

93. Somatotopy of cortico-spinal tracts in internal capsule


o corticospinal tract is in posterior limb
o face motor fibers  anteriorly
o arm and leg motor fibers  posteriorly
o lesions at this level often produce weakness of the entire contralateral body

94. Enumarate the neurocognitive functions/domains according to


DSM-5
o Delirium, Dementia, Amnestic, and Other Geriatric Cognitive Disorders

95. 2 main neuropathological markers of Alzheimer's


o Amyloid plaque
o Tau protein (neurofibrillary tangle)
-senile plaques: extracellular, amyloid beta-peptide
-neurofibrillary tangles: intracellular, hyperphosphorylated tau protein (on
microtubules)
-neuronal and synaptic loss
-inflammatory response
-vascular lesions

96. 5 modifiable risk factors for dementia associated with Alzheimer


o Diets
o Exercise
o Stop smoking
o Lower blood pressure
o Education

97. Clinical features of Brown-Sequard syndrome, due to inflammatory


lesion at T6 level
o ipsilateral spastic leg with brisk reflexes and an extensor planter response
o ipsilateral loss of joint-position sense and vibration (dorsal columns)
o contralateral loss of pain and temperature(spinothalamic tracts cross at their level
of entry

98. Clinical features of left hemisomatoagnosia


o Patient has hemiplegia and neglects the affected side of the body

99. Clinical features of tabetic dissociation and 3 possible causes


o impairment of deep sensory function, with intact thermoalgesic sensation
o paresthesias, lancinating pain, especially in lower limbs
o abolition or dimunition of reflexes
o ataxic walking
o hypotonia without atrophy
o can result in neuropathic arthropathy (charcot joints)
o causes:
1. neurosyphilis
2. diabetes
3. diseases affecting myelinated fibers from posterior columns, as in
Biermer anemia

100. Clinical features of a complete paresis of left abducens nerve


o convergent strabism
o inability to perform eye abduction
o horizontal diplopia

101. Most frequent location of berry aneurysms.


o ACA

102. Maximal duration of therapeutic window for a patient admitted


for thrombolysis in acute ischemic stroke
o 3-4.5 hours depending on which book you read

103. Classes of drugs for ischemic stroke and non-valvular atrial


fibrillation (CHADS score of 4), secondary prevention

o in chad scor of 2-6 give warfarin


o in secondary prevention give
 oral anticoagulants
 antiplatelts

104. Clinical features of a patient with ischemic stroke caused by


occlusion of the A2 segment of the left ACA
o Sensory and motor deficit in the contralateral foot and (to a lesser extent) shoulder
and hand, with sparing of the face;
o The motor deficit is more pronounced in the distal part of the lower limb
o Eyes and head may be deviated to the side of the lesion
o Patient may have urinary incontinence and contralateral grasping;
o Speech disorders may appear– especially transcortical motor aphasia

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

106. Most likely location of a lesion to manifest clinically with


fasciculation in the muscles
o Lower motor neuron lesion

107. Clinical picture in myopathy


o Aching
o Cramping
o Pain
o Stiffness
o Tenderness

108. Etiologies for differential diagnosis of ALS


o toxic
o endocrine
o neuropathies

109. On which side will appear impaired coordination of movements


in right cerebellar tumors
o Left side (contralateral side)

110. Main differential diagnosis of brain abcsess


o brain cancer

111. Macroscopic appearance and lab modifications of CSF in


tuberculous meningitis
o Increased proteins
o Increased lymphocytes
o Increased csf pressure
o Decreased glucose

112. What is the main difference between dementia and a


neurodevelopmental impairment of the cognitive function?
-dementia: the most severe expression of neurocognitive impairment. -dementia
includes cognitive disfunction is one of its symptoms (including memory loss) and
it’s not seen early in the disease

112. Treatment for trigeminal neuralgia


1. medications used: anticonvulsant drugscarbamazepine
600-1200 mg/day, gabapentin, lamotrigine
phenytoin, clonazepam, sodium valproate,
2. surgical options: radiofrequency thermocoagulation,
microvascular decompression, stereotactic radiosurgery

113. Which is the most probable diagnosis in a patient with otitis


media that develps headache and drowsiness followed by aphasia?

Cerebral venous thrombosis

114. What is asomatognosia?


a neurological disorder characterized as loss of recognition or awareness of part of the body. The
failure to acknowledge, for example, a limb, may be expressed verbally or as a pattern of neglect.
The limb may also be attributed to another person, a delusion known as somatoparaphrenia.

115. What is the treatment of a patient with status epilepticus due to


generalized tonic-seizures?

– medical emergency – life threatening condition


– Support vitals
– O2, iv line
– Short half life Benzodiazepine
– Iv phenitoin 20mg/kc (caution with cardiac block)
– Iv phenobarbital 20mg/kc
– Intubated patient – pentobarbital

116. Name 5 causes of cardioembolic stroke

-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

118. Which are the general characteristic features of meningioma?


also known as meningeal tumor, is typically a slow-growing tumor that forms from
the meninges. Although the majority of meningiomas are benign, they may have malignant
presentations. CSF protein usually is elevated if lumbar puncture is attempted. Classification of
meningiomas are based upon the WHO classification system.[19]
 Benign (Grade I) – (90%) – meningothelial, fibrous, transitional, psammomatous,
angioblastic
 Atypical (Grade II) – (7%) – chordoid, clear cell, atypical (includes brain invasion)
 Anaplastic/malignant (Grade III) – (2%) – papillary, rhabdoid, anaplastic (most
aggressive)
 Tumors originating in arachnoidian cap cells
•Represent 13-20% of intracranial tumors when they are large: Pacchioni’s granulations
 Women / men = 2/1
•Maximum incidence: 40-70 years Average age: 45 years
 CT
•Attached to dura
•Homogeneous
•Hyperdense
•Contrast Enhancement
•Variable edema
•Calcifications
•Rarely cystic
 MRI
•Dural origin
•Hyperintensity in T1
•Hypointensity in T2
•Contrast enhancement
•AngioMRI
 SURGICAL TREATMENT
•Goal : total resection

119. How can you differenciate on clinical grounds, cerebellar ataxia


from sensory ataxia?

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

123. What is the difference between a primary and a secondary dystonia?


Primary dystonia is characterized by the presence of dystonia only (tremor) (usually action
dystonia and history and clinical and lab findings are normal)
Secondary dystonia: other clinical features are present.Dystonia-plus syndromes present with a
second and relevant neurological feature: parkinsonism (dopa-responsive dystonia) or sometimes
ataxia. May be environmental (birth trauma, drug usage), psychigenic dystonia

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

125. What is the lesional significance of the absence in a patient, of the


optokinetic nystagmus?

126. Enumerate the clinical elements which support the diagnosis of


intracranial hypertension syndrome
-headache with or without vomiting, papilledema, visual disturbances

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)

128. What are the diasnostic criteria for Guillain-Barre acute


polyradiculoneuropathy?
-during first week of after onset, paraclinical tests might not be positive so diagnosis is based on
clinical grounds
-after 7-10 days: Lumber puncture (CSF analysis)- increase in protein content with normal
elements = “albumino-citologic diassociation”; some rare cases: protein content could be normal
or CSF analysis might show pleocytosis (suspect HIV infection)
-electrophysiology:
-nerve conduction studies- arguments for demyelination
-prolonged distal motor latencies (after 3-5 days)
-slowing of MCV (after 7 days)
-conduction block
- +/- sensory involvement
-needle electrode studies (after at least 10 days)
-arguments for active denervation- prognostic signs for incomplete motor
recovery due to axonal loss secondary to severe or persistent segmental demyelination
-sometimes primary axonal involvement is possible (AMAN-Ab anti-
Campilobacter jejuni and preceded by diarrhea)
-Complementary tests: -serology is rarely recommended- only if diagnosis is of doubt
-MRI may be helpful to show root inflammation
-Biopsy- rarely needed, shows multifocal demyelination and variable
degree of axonal degeneration, scattered cellular infiltrate throughout nerves and roots

129. What is the treatment for the myastenic crisis?


Breathing support: endtracheal tube, bilevel positive airway pressure, suctioning (for secretions)
Medicines: anticholinesterase medicine (for energy and stregth), immunosuppressives (slow
progession of myasthenia gravis), Igs (help immune system)
IV fluids (prevent hypotension or prevent lost fluids and electrolytes)
Plasma exchange
130. Mention at least 3 different neurological pathophysiologic conditions in
which the myotatic reflexes are abolished

131. Describe the clinical features of the Gerstmann syndrome


-finger agnosia; left-right disorientation; agraphia; acalculia
-dominant parietal lobe angular gyrus lesion (stroke or congenital abnormality)
-associated with learning dissabilities, right sided paresis and hyperactive DTR’s

132. Define brain contusion


a form of traumatic brain injury, is a bruise of the brain tissue. Like bruises in other
tissues, cerebral contusion can be associated with multiple microhemorrhages, small blood
vessel leaks into brain tissue. Contusion occurs in 20–30% of severe head injuries.

133. Enumerate general characteristics of glioblastoma


-most frequent primary cerebral tumor
-3-4/100,000/yr
-predominantly males (50-70 yr)
-CT: irregular, non-homogenous mass, found in hemispheres, contrast enhacement, peritumoral
edema, +/- intratumoral haemorrhages, no calcifications
-can cross corpus callosum (“butterfly glioma”)

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.

139. Enumerate at least 5 pathological conditions which can manifest by a


hemifacial spasm
-Bell’s palsy (idiopathic)
-tumor pressing on facial nerve
-Lyme disease
-Herpes virus
-Diabetes
-Sarcoidosis

140. What are the clinical manifestetions of a petit-mal epilaptic seizure?


-aka absent seizures
-commonly affects children (5-9) but also can in adults
-starring off into space, smacking lips together, fluttering eyelids, stopping speech in middle of
sentence, making sudden hand movements, leaning forward or backward, appearing suddenly
motionless
-no postictal confusion

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

146. How do you diagnose carpal tunnel syndrome?


-dysesthesia and pain in the fingers
-paresthesias are characteristically worst during the night
-sensory loss affecting thumb, index and middle finger
-nerve conduction studies can measure conduction speed of you nerve impulses (impulse is
slower than normal as nerve passes into the hand)

147. What is the treatment for prevention of migraine?


-if headaches are frequent, long lasting or account for a significant amount of disability
-prophylactic therapy also should be considered to prevent neurologic damage in the presence of
uncommon migraine conditions including hemiplegic migrain, basilar type migraine, migraine
with prolonged aura
-beta- adrenergic blockers (propranolol, metoprolol, atenolol, timolol)
-antidepressants (amitriptyline, venlafaxine, sertraline, fluoxetine, duloxetine)
-Ca2+ channel antagonist (diltiazem, verapamil, amlodipine)
-Antiepileptic drugs (valproate/divalproex sodium, gabapentin, pregabalin, topiramate)
149. Describe the clinical picture of an ischemic stroke in the cortical teritory
middle cerebral artery, in a right-handed patient.
-the cortical branches vascularize the lateral part of the cerebral hemispheres
-the cortex and white matter of the lateral and inferior parts of the frontal lobe (including motor
areas 4 and 6, conjugate gaze centers, Broca’s area in the dominant hemosphere)
-the cortexand white matter of parietal lobe (including primary and secondary sensitive cortex,
angular and supramarginal gyrus)
-the superior part of the temporal lobe and insular cortex including Wernicke’s area in the
dominant hemisphere)
superior trunk occlusioncontralateral sensory and motor deificit of face and upper limb and
lesser degree the lower limb; eyes and hear deviate to side of lesion; global aphasia initially (later
develops into motor aphasia)
inferior trunk occlusion predominantly expressive aphasia
150. Name the types of inflammatory myopathies that you know.
I. Inflammatory myopathies
– A. Infective or presumably infective forms of polymyositis
• Trichinosis
• Toxoplasmosis
• Cysticercosis
• HIV, HTLV-1
– B. Idiopathic polymyositis and dermatomyositis – usually
associated to connective tissue disorders affect primarily
striated muscle and skin
• Sometimes paraneoplastic syndromes
• Only DM affects children
• Diagnosis based upon specific changes in muscle and skin
biopsy
– C. Inclusion body myositis (IBM)
• Predominates in males
• Onset in middle or late adult life, more frequent than PM
• Diagnosis based on intracytoplasmatic vacuoles and congophilic inclusions in
both cytoplasma and nuclei of degenerated muscular fibers

152. How do you define dystonia ?


A PERSISTENT ATTITUDE OR POSTURE PRODUCED BY COCONTRACTION OF
AGONIST AND ANTAGONIST MUSCLES THAT PLACE THE LIMB IN AN UNNATURAL
POSITION
• OVEREXTENSION/ OVERFLEXION OF HAND
• INVERSION OF THE FOOT
• LATERAL FLEXION OR RETROFLEXION OF THE HEAD
• FORCEFUL CLOSURE OF THE EYES
153. What is the main ocular sign in wilson's disease ?
Wilson's disease is a genetic disorder in which copper builds up in the body.
A brown ring on the edge of the cornea (Kayser–Fleischer ring) is common in Wilson's disease,
especially when neurological symptoms are present.

154. How do you treat patient with myasthenic crisis ?


-Careful intubation followed bye mechanical ventilation.
-anticholinesterase drugs withdrawn.
-PE or IV Ig – hasten improvement.
155. Which is the acute treatment for a patient with cerebral sinus thrombosis
and associated hemorrhagic infarction?
-Acute anticoagulant treatment
-Management and prevention of early complications:
1)Elevated intracranial pressure and herniation
2)Seizures
-Antibiotics +/- surgical drainage of infectious sources (where the case)
-Analgetic treatment for headache

156. Enumrate the types of clinical manifestations in vertebro-spinal trauma ?

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

158. 28 ) Define the cerebral secondary tumors?

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.

161. The optokinetic nystagmus is present in normal or pathological


condition?
Optokinetic nystagmus (OKN) is nystagmus that occurs in response to a rotation movement. It is
present normally. The optokinetic response is a combination of a slow-phase and fast-phase eye
movements. It is seen when an individual follows a moving object with their eyes.

162. What is the locked – in syndrome?


LOCKED – IN STATE = an awake patient has no means of producing speech or volitional
movement, but retains vertical eye movements and lid elevation ->MORSE CODE .

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

164. what type of paraclinic investigation is mandatory for diagnosis of


multiple sclerosis?
Diagnosis was based on Charcot triad consisting in nystagmus, intention tremor, and telegraphic
speech(scanning speech).
165. What are the oculo-cephalogyric and acoustico-cephalogyric movements
and which is the anatomical-functional substrate of their production?
Are automatic movements that means turning of the eyes and head toward the source of an
auditory,visual,or other form of stimulation.
They are used to determine whether the brainstem is intact.
Lecture: oculocephalic reflexes = doll’eye movement
!Not present in a normal alert person // absence= damage within the
brainstem
- oculovestibular or caloric response // absence =
damage within the brainstem

166. How would the corneal reflex be modified in a pyramidal syndrome ( on


the affected side)?
The corneal reflex involves asking the patient to look away from the examiner which later on is
followed by touching the cornea of the patient with piece of cotton , normally both eyes close
together ,but in a patient with upper motor neuron or pyramidal syndrome there will be a delay
in closure of the opposite eye (decreased speed of closure).

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

168. What disease is typically associated with the pseudohypertrophy of the


calves?
DUCHENNE PROGRESSIVE MUSCULAR
DYSTROPHY
DMD =group of striated muscle degenerative disorders,
genetic conditioned – impairment of dystrophin – gene –
Xp21

169. Name three causes of isolated involvement (mononeuropathy) of the


common peroneal nerve.
Causes :
– Pressure palsy spontaneous or associated to
HNPP (hereditary neuropathy with pressure
palsies)
– Diabetic neuropathy
– Fibular bone fractures
– Hematomas around the fibular head
170. Which are the tests for paraclinical diagnosis of myasthenia, and how are
these results interpreted to support this diagnosis
Diagnosis
• Measurement of receptor antibodies in blood – sensitive and highly specific test
– RIA is the method of choice
– 80-90% of patients with generalized myasthenia and 60% of those who are restricted to ocular
muscles
– Seronegativity does not imply clinical or electrophysiological differences
Pharmacologic tests
• Use of edrophonium or neostigmine
– Test a group of muscles or determine vital capacity and then inject the substance and
depending on the half-life the test is redone at a certain time interval
– If significant, visible improvement in strength occurs we consider the test positive for
myasthenic deficit.
Electrophysiology
• Nerve conduction studies and EMG are both normal in myasthenic patients
• Repetitive nerve –muscle stimulation
– Rapid reduction in amplitude of compound muscle action potentials after 3/sec
stimulation of a peripheral nerve –
– decremental response and reversal of this response by anticholinesterase drugs is a
reliable confirmation of diagnosis

171. What is the most frequent type of focal epilepsy in adults


Focal (partial) seizures – consciousness retained, patient able to
describe the clinical content of his seizures
– Simple focal seizures
– Complex focal seizure
Most frequent is Complex partial seizure

172. What is the recommended management in case of a patient present in the


emergency room for an epileptic seizure ( the first in his life)?
*Acute treatment of a seizure:
– Check vital functions and start support if needed
– Iv. Benzodiazepine with short T1/2 (diazepam, lorazepam)
* Status epilepticus: seizing for more then 30 min.
• Generalized tonic-clonic status – medical emergency – life threatening condition
– Support vitals
– O2, iv line
– Short half life Benzodiazepine
– Iv phenitoin 20mg/kc (caution with cardiac block)
– Iv phenobarbital 20mg/kc
– Intubated patient – pentobarbital

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

177. Define the simple febrile seizures


1. Generalized
2. Lasting less than 15 minutes
3. Do not reccur during the same illnes
Common seizure type: generalized tonic-clonic, but can be atonic, tonic.
Most “simple FS” are of short duration: 3-4 minutes .
Children quickly retake previous activities after simple FS.
Prolonged drowsiness is not typical for simple FS.

178. What is pavor nocturnus?


DEFINITION:
Recurrent episodes of suddenly, incomplete awakening in the first 1/3 of
sleep
 from stage III to stage IV of non REM sleep

Onset: 18 mo -5 ys,
Disappear: spontaneously →12 ys old;
CLINICAL ASPECT:
Suddenly sitting, crying, agitation;
Eyes are opened, fixed, terrified;
The child is moving, speaks non
-intelligible or pronounces phrases related to events of the day;
He cannot recognize his parents;
Cannot be awakened from the parents;
Vegetative elements: pale / cyanosis, tachycardia, mydriasis, dyspneic
breathing, increased muscle tone;
1-10 min;
 He falls asleep;
 Not remembering the episode;
Treatment:
In general not necessary;
If frequent episodes –benzodiazepines;

179. Explain how interstitial cerebral edema appears.


A drop in CBF < 10-12ml/100g/min leads to infarction, depending of the duration of ischemic
injury

A CBF of 6-8 ml/100gr/min :


severe depletion of ATP, ↑ K extracellular, ↑ Ca intracellular, cellular acidosis histologic
signs of necrosis
pPhospholipases are activated –destruction of neuronal membranes
Prostaglandines, Leukotrienes, Free radicals accumulate intracellular enzymes and proteins
are altered
Neuronal ballooningcytotoxic edema

180. Name the key aspects of migraine in children


 Migraine headaches are the most common acute and recurrent headache pattern
experienced by children. These often incapacitating experiences are noteworthy for their
sudden onset and accompanying symptoms of nausea, abdominal pain, vomiting, and relief
by sleep.

181. What stimulating procedure triggers the typical absence of childhood?
PRIMITIVE REFLEXES
Or EEG
 The background must be normal
 Regular 3 Hz generalized spike-and-wave occurs associated with
absence seizures. Polyspike-and-wave can occur in the ictal EEG.
 EEG abnormality and absence seizures are provoked by
hyperventilation
MRI
 Normal
 Not always required

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

184. Define cerebral dilacerations and name the main types.


Is a primary traumatic effect is a type of traumatic brain injury that occurs when the tissue of the
brain is mechanically cut or torn
- the injury is similar to a cerebral contusion; however, according to their respective definitions,
the piaarachnoid membranes are torn over the site of injury in laceration and are not torn in
contusion
_ Lacerations require greater physical force to cause than contusions
_ coexist with other primary effects such as brain contusion and / or side effects such as
posttraumatic subdural hematoma, extradural etc. direct and indirect. Quest.

185. Define pseudotumor cerebri


idiopathic intracranial hypertension

186. What are the clinical and paraclinical criteria necessary for the diagnosis
of cerebral death?

BRAIN DEATH - CRITERIA


• Coma of a known cause
• Absence of motor responses
• Absence of brainstem reflexes (pupillary, corneal, caloric, gag)
• Absence of coughing in response to tracheal suction
• Absence of respiratory drive at a PaCO2 – 60mmHg or 200mmHg
above baseline= APNEA TEST
• Interval between exam – usually 6h
• Perform confirmatory tests – cerebral angiography
• EEG – recording are obtained for at
least 30min with a 16-18 channel
• TCD – both MCA and AV
• nuclear imaging with technetium
187. Name 4 types of causes fo cerebral palsy, at least on for each category –
spastic –ataxic -dyskinetic ?

Ataxic CP(Extrapyramidal CP)


• Condition that occurs when there is damage to the
cerebellum (which normally regulates balance and
muscle coordination). Ataxic cause: premature birth
Athethoid /Dyskinetic /Extrapyramidal CP
• A condition that occurs when there is
damage in the basal ganglia → results in an
overflow of motor impulses to the muscles →
abnormal regulation of tone, ---athetoid,dystonic – cause :birth asphyxia
Spastic CP (pyramidal)
• Result from damage to motor areas of the
cerebrum; --- hemiplegia ,diplegia ,quadriplegia cause: stroke ,IVH

188. What are the criteria for positive diagnosis for type I spinal amiotrophy
( werdnig Hoffman disease?

SMA type I - Werdnig-Hoffmann


• antenatal onset– absence of fetal movements
• floppy child syndrome– generalized hypotonia
• Batrachian, frog-like position
• Decreased proximal muscle force
• Diminished active movement
• Absent osteotendinous reflexes
• Tongue fasciculations
• Difficulty sucking and swallowing
• Abdominal breathing
• Facial mimicry intact = cognitive development is normal
• Head control – not achieved
• Death < 2 years of age

189. What is the clinical difference between a vegetative state and minimally
conscious state ?

VEGETATIVE STATE= awake but nonresponsive state


• Yawning, coughing,swallowing and limb and head movements persist =
awake coma. Respiratory and autonomic functions are retained.
• These people have emerged from coma after a period of days or weeks
• AKINETIC MUTISM = partially or fully awake state in which patient is
immobile and mute
• Lesions situated on the orbitofrontal surfaces
A minimally conscious state (MCS) is a disorder of consciousness distinct from persistent
vegetative state and locked-in syndrome