CASE 1: Male, 65 years old, was delivered to a hospital due to weakness in his left CASE 2: Male, 65 years old

s old complains of shaking and stiffness in the extremities, more

extremities, which developed 2 hours before hospitalization. present on the left side. The patient considers himself ill for 5 years, from the time the
shaking and stiffness first developed in his left hand. In course of gradual progression of
Anamnesis morbi: The patient has a long time history of angina of effort, within last the disease stiffness in the left leg joined and later shaking and stiffness appeared in his
year there was a number of incidents of blood pressure increase up to 180/100 mm Hg. right hand. Within the recent time the patient noticed the motor symptoms severity
Within the last 3 months the patient experienced a number of short time episodes of fluctuation developed in relation to the Levodopa intake - hyperkinesis resembling chorea
transient right eye blindness .Upon examination: Patient is in clear consciousness, arterial appear within a short time after the first daily dosage but cease soon being substituted by
blood pressure is 180/100 mm Hg, hart rate - 80 per minute, regular hart rhythm, marked dystonic spasms observed preferably in legs.
decreased carotid artery pulsation on the right side, but increased temporal artery
pulsation on the same side. Neurological status: hypomimia, dysartria, hands tremor resembling "coins
counting" (more present on the left side), muscle tone increase with the "cog wheel"
Neurological status: no meningeal symptoms, weakness of the lower portion of phenomenon, movement speed is decreased; rigidity and hypokinesia are found in the
the mimic muscles on the left side, deviation of tongue to the left side, decreased left leg; the patient's gait reveals the absence of the physiological synkinesias in the left
muscle strength in the left hand up to grade 1, in the left leg up to grade 4, tendon hand and shuffling of the left leg; the tendon reflexes are of the mild agility,
reflexes are increased in the left extremities, left side Babinsky sign. symmetrical, no pathological reflexes found.
Common blood test: no changes.
ECG: sinus rhythm, no signs of focal myocardial ischemia. Common blood test and biochemical blood analysis: no changes.
CT scan: no changes of brain matter`s density Duplex ultrasonography of carotid and vertebral arteries: no signs of stenosis
MRI of the brain: no focal changes (see pic.)

1.Neurological syndromes and topical diagnosis?

 Left side central hemiparesis (precentral gyrus, internal capsule and
corona radiata at R side)
 Left side central of mimic muscles of the tongue (R corticonuclear tract)
 Lesion: corona radiata/ internal capsule (more commonly affected

2.Preliminary clinical diagnosis? 1. Neurological syndromes and topical diagnosis?

- Atherothrombotic type of ischaemic stroke (internal carotid a. occlusion)  Hypokinetic - hypertonic movement disorder.
3.Treatment?  Localisation: neurodegeneration in substansia nigra ( decreased dopamine
 antiplatelet – dabigatran release
- These are better to control – don’t have to use INR (international normalized 2. Preliminary clinical diagnosis?
ratio) - Parkinson’s Disease
- Adverse effect: Bleeding 3. Treatment?
 Dopamine agonist :Miraplex (6mg), Pronoran (50-150mg)
 Thrombolysis treatment – within 3 hours penumbra zone (+altepase)  Levadopa + carbidopa
 Anticoagulant (aspirin, clopidrogrel)  MAO-B inhibitor: Selegiline (5mg)
 Monitor BP  Increase dopamine release: Amantadin, Amytriptilin
 Antihypertensive drugs – ACE- I: perindopril (c/I: renal artery stenosis, A/E: dry  COMT inhibitor: entacapone, tolacapone
cough), CCB: Amlodipine, beta blocker: labetolol/bisoprolol (c/i: asthma and  Anticholinergic drug: Trihexyphenydyl, benzotropine
bradycardia; A/E: diabetic)
 Stenting
CASE 3: Female of 54 years old complains of the leg weaknesses, walking difficulties, CASE 4: Male of 40 years old complains of pain, tingling and burning sensation in his
"pillow-like" feeling under her feet. These complaints first appeared a number of months both feet as well as gait unsteadiness.
ago and gradually increased since then.
Upon neurological examination: "socks-like" pattern of all types of sensation
In the anamnesis: 10 years ago the patient was diagnosed with anemia of an decrease, decreased knee reflexes, achillis reflexes are absent, the patient stays in the
unclear genesis with the blood hemoglobin decrease to 60 g/L. She took ferrum Romberg test and when walking, which remarkably increases when he closes the eyes.
containing medication and vitamin B12, which led to the normal level of the blood Muscle strength is normal. No disturbances of pelvic functions.
hemoglobin. Within a number of years the blood test was not performed. Common blood test: no changes.

Upon neurological examination: weakness of the leg muscles up to grade 4, ECG: sinus rhythm, no signs of focal myocardial ischemia.
muscle tone is slightly decreased, knee and achillis reflexes are decreased, Babinsky sign Electroneurography: conduction velocity in n. peroneus is 43 m/s and in n. tibialis – 40
is found on both sides; can hardly identify the direction in which her toes are moved to as m/s, amplitude of muscle decreases essentially.
well as the movements in the ankle joints, the 2 dimensional sensation in legs is Needle electromyography: single fibrillation potentials (see pic.)
decreased, vibration sensation on the iliac spine and the hip joint is decreased and is What causes polyneuropathy:
absent on the ankle joints, the heel- knee test is performed with the goal missing; the 1. Diabetic
patient is unstable in the Romberg posture and when walking, more markedly with the 2. Thyroid gland disturbances:
closed eyes. hypothyroidsm
3. Alcoholism
**Pillow like feeling: symptom of sensory ataxia
4. Autoimmune
Common blood test: signs of pernicious anemia 1 .Neurological disorders?
5. Hereditary
Biochemical blood analysis: no changes. • Sensory ataxia,
Duplex ultrasonography of carotid and vertebral arteries: no • Polyneuropathy + parasthesia, type of sensory disturbances (neuropathic pain)
signs of stenosis 2. Localization of the lesion?
MRI of the brain: no focal changes (see pic.)  Distal peripheral nerve (n. peroneus and n. tibialis)
1.Neurological syndromes?  Myelin sheath: Axonopathy due to demyelination ( decrease velocity and
 Sensory ataxia (proof: Pillow like feeling, decreased sensation, Romberg amplitude in EMG)
test and heel knee test missing goal)  MOI: Anamnesis:
 Spinal conductive type of deep sensory disturbance  what drug are they taking (chemotherapy drug, antiarrythmic drug,CCB), history
 Central and peripheral paraparesis ( +ve Babinsky sign, decreased reflex (for hereditary)
and muscle tone)  Glycated hemoglobin, glucose lvl, creatinine level, electrolyte level
2.Topical diagnosis?  Throxine and T3 lvl
- Lateral fasiculus of corticospinal tract  Ultrasound for thyroid
- Posterior column of spinal cord ( thoracic part: as both leg affected)  Alpha 1, alpha 2 globulin
- Internal capsule and corona radiate, precentral gyrus  Lumbar puncture
3.Preliminary clinical diagnosis and additional methods of investigation?
 Dx: Funiculus myelosis, subacute combied degenerative of spinal cord 3. Treatment?
(vitamin B12 def)  -Lipoic acid (for polyneuropathy)
 Additional Ix: CBC, MRI thoracic part, sensory evoked potential/  Physical exercise
transcranial magnetic stimulation (if we dunno his history)  Control glucose level
4. Treatment?  Immunoglobulin (for autoimmune)
- vitamin B12 (IM) – 500 mg per day for one week  vitamin B1, B6
- Folic acid  Tx for pain: antidepressant-amitriptyline, antidepressant- valproate,
- Alpha lipoid acid toperamide, NSAID< opiates
CASE 6: A man, 72 years old has pain and skin rash on the right frontal area, which Common blood test: no changes.
appeared 5 days ago. The last several years he had arterial hypertension ( max up to ECG: sinus rhythm, no signs of focal myocardial ischemia.
150/90 mm ). CT scan: focus of hyperdensity signal
In neurological examination: there is vesicular eruption on the skin on the right frontal
area, decreased temperature and pain sensation, no other neurological symptoms.
Localisation of sensory disturbances in the picture (area a):

Stripe: Sensory problem

Segmental radiculo type of
sensory disturbances

1. Neurological syndromes and topical diagnosis?

Neurological Syndromes
1. Neurological syndromes? - meningeal syndrome
- Trigeminal neuralgia (first branch of trigeminal nerve: ophthalmic) - Left-sided central hemiparesis (lesion in frontal lobe and corona radiate)
- Segmental radicular type of sensory disturbances - Central paresis of facial n (?)
- Loss of consciousness
2. Topical diagnosis? - Generalized seizures
Acute Herpes Zoster (proof: vesicular rashes and pain and numbness) - Gaze center – coordinate eye movements in pontine and frontal lobe
 Oculomotor nerve:
3. Preliminary clinical diagnosis and additional methods of investigation?  Eye movement innervate m. rectus superior, inferior, medialis (when right
MOI: Serologic test eyes move towards the nose – inward)
 Abduscens nerve – lateral left eyes move outwards (m. Rectus lat)
4. Trearment?
- antiviral drugs – acyclovir 2. Preliminary clinical diagnosis and it’s pathogenesis?
- anticonvulsants  Intracerebral hemorrhagic stroke due to cocaine abuse
- antidepressants: Amitriptyline  Tonic clonic seizure (hematoma and cause brain edema, increase in ICP,
It should be treated properly to prevent postherpetic neuralgia dislocation of brain structure)
 Hematoma localized in thalamus, pons and cerebellum

3. Treatment?
 Decreased brain edema: mannitol, glycerol
CASE 7: A man of 26 years was hospitalised because of the acute weakness in left  Surgery to remove hematoma
extremities and loss of the consciousness. He has drug abuse of cocaine. During last three  Neuroprotective drug
months he had 3 attacks with loss of consciousness and tonic-clonic siezures.  Control BP
In neurological examination: he is in sopor, he has rigidity of cervical muscles and Main cause of haemorrhage
positive Kernig sign at both sides, eyes are turned to the right, the weakness of the left - Arterial hypertension
lower part of face, no activity in left extremities, on the left side high reflexes and positive - Rupture of vessels
Babinsky sign. - Bleeding into parenchymal of brain and ventricle
 CASE 9: A man of 60 years has behavioral abnormalities: apathy, loss of interest to the
CASE 8: A man 32 years has seizures with the loss of consciousness. He had a car accident surrounding world and critic to his behavior, which was appeared 1 year ago and
at 6 months ago, when he lost the consciousness for a long time. 3 months after car increases during time. Because of these symptoms he could not do his professional duties,
accident he had the first tonic-clonic seizure with lose of consciousness and urinary and had to retire on a pension. During last time there are episodes of urinal incontinence.
incontinence. The same attacks are repeated every 2 weeks. In neurological observation In neurological examination: low intellect, dynamic praxis, impulsivity by making decisions
there are high reflexes, positive Babinsky sign at right side . and perseverations. The patient has no paresis, no sensory disturbances and other
neurological syndromes.
Common blood test: no changes.
ECG: sinus rhythm, no signs of focal myocardial ischemia. Common blood test: no changes.
CT scan: low density focus in brain matter (see pic.) Biochemical blood analysis: no changes.
ECG: sinus rhythm, no signs of focal myocardial ischemia.
Duplex ultrasonography of carotid and vertebral arteries: no sighs of stenosis.
MRI of the brain: signs of internal and external hydrocephalus predominantly in anterior
parts of the brain (see pic.)

1. Localisation of lesion?
 Frontal lobe (emotions, speech), temporal (speech)
2. Preliminary clinical diagnosis?
Frontal temporal dementia
 Behavioural changes, preservation
 Pressure hydrocephalus
- Hakim Adam’s triad
o Frontal ataxia, gait (pt x)- medial side of hemisphere
1.Neurological syndrome, type of seizure? o Urinary disturbances (incontinence)
1. Right pyramidal syndrome o Behavioural changes
2. Generalised tonic- clonic seizures, Treatment: shunting
3. Post traumatic epilepsy with generalized tonic-clonic seizures  due to mild - MRI : Asymmetrical frontal lobe ( atrophy)
concussion after 3 months, then he has repetitive seizures
3.Treatment and prognosis?
2.Topical diagnosis? - mimantin – not very effective
 Left sided mild concussion ( Lesion: cerebral cortex – frontal lobe) - antidepressants – decrease levels of serotonin
- fluoxetine – can control food problems better
3. Preliminary clinical diagnosis?
 Post. trauma epilepsy, brain cerebral concussion -disease starts after 40, sometimes hereditary
-problems with mood, memory, gnosis, praxis
4.Treatment? - anxiety
- Anticonvulsant ( valproate,Transquilizers) - loss of emotional control
- Control with EEG - increased sexual activities
- say things without thinking
- hyperglycemic – increased appetite, bulimia, eat sweet things in huge amount
CASE 10: A woman of 45 years has uncontrolled fast movements in face and extremities, CASE 11: A female patient of 72 years and suddenly felt an intensive headache in the
which appeared 2 years ago and become stronger. Her mother had the same symptoms at occipital region accompanied by vomiting and photophobia. She was urgently delivered
40 years, which progressed and were accompanied by gait abnormality and dementia and her to a hospital by ambulance.
she died at 55 years. Before the illness the patient considered herself practically healthy, with usual
blood pressure of 120/80 mm Hg.
The neurological status: there are uncontrolled movements in face, body and Upon examination: patient is in clear consciousness, arterial blood pressure -
extremities, she likes to a “dancing women”, the muscle tone and reflexes are normal, no 150/90 mm Hg, heart rate- 88 per minute, regular heart rhythm.
pathological signs. Neurological status: neck muscles rigidity, no paresis or any other neurological
Common blood test: no changes. disorders.
Biochemical blood analysis: no changes.
ECG: sinus rhythm, no signs of focal myocardial ischemia. Common blood test: no changes.
Duplex ultrasonography of carotid and vertebral arteries: no sighs of stenosis. ECG: sinus rhythm, no signs of focal myocardial ischemia.
CT scan: increased density of signal in area of basal cistern and lateral fissure (see pic.)
1. Neurological syndromes?
o Hyperkinetic – chorea
o Hypotonic
# Hyperkinetic- hypotonic movement disorder

2. Clinical diagnosis?
o Huntington disease (prove it!)
a. Hereditary – increased repetitive trinucleotides repeats 3 times
b. Cognitive decline dementia
1. Neurological syndromes?
c. Chorea
1. Photophobia
d. Gait
2. pulsating and vibration headache
e. Behavioural changes
3. Meningeal syndrome (?)
3. Treatment and prognosis?
2. Clinical diagnosis?
- MOI
 Migrane without aura (proof: Photophobia, vomiting, headache)
- Genetic test
 Subarachnoid hemorrhage
- General investigation
 Treatment
3. Treatment and prognosis?
a. Symptomatic
 Triptans – 5HT1 Serotonin receptors agonist : Sumatriptan, Naratriptan,
b. Benzodiazepine
Zolmitriptan
c. Antidepressants (chorea TX)
 Ergotamine derivatives: ergotamine gidrotartrat (kofetamin, kafergot,
d. Selective 5HT receptors
kaffetin) dihydroergotamine (digidergot).
e. Atypical neuroleptics – Olanzapine (GS), Clozapine
 Antiemetics: metoclopramide, domperidone
f. Tetrabenazine – decrease DA transmission
g. Hantexil – antagonist of DA receptor (A/E: parkinsonism)  Prevention of Chronic attacks: beta blocker, antidepressant, CCB
h. stimulate glutamate transmission (verapamil), antiepileptic (topiramide), vasoactive drug

-Bad prognosis
CASE 12: A female of 50 years old complains of diffuse headache of squeezing character CASE 13: A male of 45 years old experienced an attack of a low back pain during physical
which feels like as if "her head is tightened with a band". The patient has been suffering load when working in his countryside house. The pain irradiated over the back-lateral
from this headache since 30 years, but within last year they became constant. The patient surface of his right leg and did not regress. On the 4-th day the patient saw a doctor.
When questioned, the patient mentions that his pain increases with any movement in the
had to take 1-3 tablets of analgesics (pentalgin, spasmalgon etc.) per day with no effect.
low back region, as well as cough and sneezing.
Physical load does not influence the character of the headache, no vomiting and nausea,
no photo- and phonophobia. There is no family history of headaches. Upon neurological examination: marked tension of the back muscles, lumbar
Upon examination: pain in the pericranial and neck muscles caused by palpation, region scoliosis curved to the right, flatness of the lumbar spine region. Movements in the
no focal neurological signs revealed. low back region are markedly decreased, bending forward and sidewards are not possible
because of sharp pain increase. Pain hypoestesia over the external surface of the right
Common blood test: no changes. calf and the external margin of the right feet; the Achillis reflex is absent on the right
Biochemical blood analysis: no changes. side, positive Lassegue symptom from the 30° angle.
ECG: sinus rhythm, no signs of focal myocardial ischemia.
Duplex ultrasonography of carotid and vertebral arteries: no sighs of stenosis Common blood test and biochemical blood analysis: no changes.
MRI of the brain: no focal changes (see pic.) ECG: sinus rhythm, no signs of focal myocardial ischemia.

1. Clinical diagnosis? 1.Neurological syndromes?

Tension- type headache (Drug induced headache) - Acute vertebral lumbarishalgia
Proof: Diffuse headache of squeezing character (band-like feel), chronic form of -Pain syndrome
headache (30 years) - vertebral muscle-tension syndrome of the para vertebral muscle
-vertebral syndome
2. Are any additional methods of investigation necessary? - Scoliosis
- keep a headache diary (record frequency of headaches per month), CT(if got tumour) - Flatness of lumbar spine region
# It’s important to know about the history of patient - Segmental radiculopathy

3. Treatment? Taking medicines more than 3 days a 2.Lesion localization?

Drug therapy Nerve root (L5 – S1)
week may lead to rebound headaches.
 Non-narcotic analgesics
These are headaches that keep coming
 Antidepressants 3.Clinical diagnosis?
o Amitriptyline back due to overuse of pain medicine.
Segmental Radicular type of sensory disturbances
o SSRIs (fluoxetine, fluvoxamine)
o SSNRIs (venlafaxine, milnacipran, duloxetine) 4.Treatment?
 Atypical benzodiazepines: alprazolam - Bed rest for 1 week
 Muscle relaxants: sirdalud - No sudden movement
 Steroid in morning - Analgesic – 1 week
Drug-free treatment - local inflammation near nerve root compression
 Massage o Vasogarlio? Pentoxyphillin, Diazepam (IV) – to decrease pain
 Physiotherapy - steroids and local anaesthetic
 Botulinum toxin

# Rebound HA is treated with baclofen, tiazipine, detoxification with

prednisolone
 Indication for neurosurgical treatment
Cauda equine compression (actue situation)
Urinary disturbances (retention) – Paresis
Perform non-invasion procedure but pain still persists. White area near the ventricles:
signs of neurkaryosis-
MOI
demyelination of
MRI – to find out herniation and how to compress
EMG – F-wave – decrease if patient has radiculopathy Examine his neuropsycological
Increased patient cough, sneeze and bend forward – abdominal pressure state
increase (space between vertebrae increases, thus can stop compression for a
short period of time)
1
- Increase compression of nerve root
1. Preliminary clinical diagnosis?
Red flags
 Neurogenic syncope (orthostatic syncope)
Corticosteroids
 Orthostatic hypertension (how to test: lying position after 10-15mins then take
o Side effect: Osteoporosis
the blood pressure and pulse, Pt will stand, record the blood pressure and pulse
Fever
in 1-3 mins:  . Normally the shouldn’t be a diffenrence but if there is a
Increased erythrocytes
difference of BP, if systolic is more than 20mm/Hg, and diastolic goes  more
Spondyloarthritis
than 10mm/Hg , the probe is positive and patient will get hypotension.

2.Possible reasons of his condition and additional methods of investigation?

CASE 14: A male of 65 years old has been suffering from arterial hypertension and  Possible reasons: Diabetes mellitus (dysmetabolic) , arterial hypertension
diabetes mellitus 2 type for a long time. In the morning he fell after an abrupt rise from (vascular)
his bed and lost consciousness. He was unconscious during several seconds. Within a  Additional Ix: MOI: Electroencephalography, EEG-video monitoring,
number of last month he periodically noticed dizziness and feeling of being about to lose echocardiography, CT scan, MR-angiography
consciousness after an abrupt rising from his bed or chair.
3. Treatment?
Upon examination: complains of decreased concentration of attention, slowness of • increased intake of fluid and salt (3-4g)
thinking. Arterial blood pressure in sitting position is 140/90 mm Hg, in vertical position it • mineralocorticoids (Fludrocortisone) – it will increase bp, give
decreases to the level of 90/60 mm Hg and within 5 minutes reaches the level of 100/70 antihypertensive
mm Hg. Neurological status: no pathological changes.
• -agonists (midodrine)
• Nitroglycerine
Common blood test and biochemical blood analysis: no changes, except
hyperglycemia (fasting glucose level 8,0 mmol/l).

ECG: sinus rhythm, no signs of focal myocardial ischemia.

Duplex ultrasonography of carotid and vertebral arteries: atherosclerotic stenoses of
carotid arteries up to 30 % of diameter both sides.
On MRI the following changes (see pic.):
CASE 15: A male of 39 years old with a long time history of alcohol abuse during his 1. Neurological syndromes and topical diagnosis?
drinking session developed general weakness, anorexia, abdominal pain, repetitive
vomiting and diarrhea. These disturbances lasted for several days after the patient a) Neurological Syndromes
- Cerebellar ataxia – usually mixed (cerebellar + sensory): cerebellum and
stopped taking alcohol. In the end of this period they become accompanied by double
vestibular nucleus connection lesion, due to alcohol abuse
vision and gait disturbance. He urged for medical help and was urgently admitted to a - Ophthalmoplegia:
hospital with a suspected stroke.  Diplopia – double vision
 Strabismus – Convergent (Abduscens nerve palsy – bilateral): pons
Upon neurological investigation: the patient is conscious but disoriented in time - Amnesia (korsakoff syndrome)
and space, current and long term memory is severely disturbed, no meningeal symptoms, - Polyneuropathy – type of sensory disturbances LMN lesion of spinothalamic
convergent strabismus, limitation of horizontal gaze to the lateral sides (both eyes), tract, superficial sensory disturbance (medial thalamic nucleus)
horizontal and vertical nystagmus, muscle strength is sufficient in all limbs, muscle tone
and reflexes are decreased, "socks" and "gloves" pattern of pain and temperature b) Topical Diagnosis
sensation disturbances; the patient can not sit and stand independently due to the  Medial Thalamic Nucleus
balance disturbance.  Reticular formation of midbrain

ECG: sinus rhythm, no signs of focal myocardial ischemia. 2. Clinical diagnosis?

On MRI the following changes (see pic.): lesion in corpus callosum of hypothalamus,
lesion in pons (abduscens nerve)  Wernicke Encephalopathy
- Caused by lack of thiamin – B1 vitamin def. – loss of consciousness of
different range, and withdrawal syndrome

3. Treatment and prognosis?

a) Stop alcohol
b) Improve diet
c) vit B1 (1m) Thiamin First in tablets for very long period (A/E: fixation
amnesia—cant rmb thing in just time)
d) Antidementia drugs – Mimantin
e) NMDA receptors
f) Inhibitors of acetylcholinesterase
CASE 16: Patient C. of 72 years old with a long time history of arterial hypertension and 1. Neurological syndromes and topical diagnosis?
widespread atherosclerosis suddenly felt weakness in the right hand and, to the less Neurological Syndromes
extent, in the right leg, difficulties in choosing the correct world in conversation. - Right side central hemiparesis, predominantly in leg
- Central mimic muscles and tongue paresis
Upon neurological examination: the patient is in clear consciousness, is oriented - Sensory aphasia
in time and space, reacts adequately, carries out all requests and instructions of his
physician. The patient's speech is markedly disturbed: he says only separate word Topical Diagnosis
between which he keeps long pauses, the words are not grammatically connected to each - Post limb of Ant 2/3 of Internal Capsule + Corona Radiata (Left side)
other. He uses predominantly nouns, some time pronounces them incorrectly: it's not - Wernicke area (post sup temporal lobe)
rare that he repeats separate phonemes or syllables of the word he wants to say (for
example, he says "rukur" instead of "ruka", etc.). Same type of mistakes is made in 2. Clinical diagnosis?
sentence or long words when he repeats them after his physician. Attempts to express - Acute Ischemic Stroke
his thoughts in writing are also unsuccessful. - Atherothrombotic Subtype (Left Middle Cerebral Artery)

The neurological status examination reveals central mimic muscles and tongue 3. Treatment?
paresis on the right side, right side central hemiparesis with muscle weakness expressed - thrombolytic
more in his leg that in his hand. - stenting therapy
- Anticoagulants: Aspirin, clopidogrel
Common blood test and biochemical blood analysis: no changes. - hypotensive therapy
ECG: sinus rhythm, no signs of focal myocardial ischemia. - Surgical
Duplex ultrasonography of carotid and vertebral arteries: atherosclerotic stenosis of left - Carotidectomy (big source of recurrent stroke)
internal carotid artery up to 90 % of diameter.
On MRI the following changes (see pic.):
CASE 17: A young man of 23 years old applied to a clinic with the complaints of hands
shaking and blurring speech. The patient considers himself ill for one year.
Upon neurological examination: no paresis, no sensory disturbances, muscle tone
is decreased, high amplitude postural-kinetic tremor in hands. He attracts specific
attention by his uninhibited behavior, loss of the sense of social distance in
communication with his physician. It is known that the patient's brother died of hepatic
cirrhosis in the age of his teens.

Common blood test: no changes.

ECG: sinus rhythm, no signs of focal myocardial ischemia.
Ultrasonography of abdomen: increased size of liver.
On MRI the following changes (see pic.):
 CASE 18: A male of 27 years old become a car accident victim. At the accident time he was
inside the car and hit his head. The head trauma caused loss of consciousness lasting for
about 5 minutes, after which there was one episode of vomiting. The patient is admitted
to a hospital within an hour after the trauma.
The patient complains of headache, dizziness and nausea. He does not remember
the circumstances that accompanied his injury.
Neurological status: the patient is disorientated in time and space, no meningeal
signs are detected, spontaneous horizontal nystagmus in both eyes, tendon reflexes in
his left extremities are increased, positive Babinsky sign on the same side.
Common blood test and biochemical blood analysis: no changes.
ECG: sinus rhythm, no signs of focal myocardial ischemia.
On MRI the following changes (see pic.):

1. Neurological syndromes?
- hyperkinetic
- hypotonic
- tremor
- dysarthria

2. Clinical diagnosis? 1.Preliminary clinical diagnosis?

- Wilson’s disease – because of hepatic cirrhosis  Mild contusion (frontal lobe predominantly on the right side).
- Kaiser Flescher ring – seen with slit lamp  Left pyramidal syndrome (+Babinsky sign& hypereflexia), w/o central
- copper accumulation in basal ganglia, kidney (renal insufficiency), liver hemiparesis due to x weakness
- Basal ganglia – cognitive decline, emotional symptoms (depression, anxiety,  Reterograde amnesia: cuz he doesn’t remember the circumstances that
aggression), psychosis, behavioural changes, if young age can be mental accompanied his injury.
retardation  Vestibular and cerebellar ataxia ( horizontal nystagmus)
 Mild focal symptoms (headache, dizziness, nausea and vomiting)
3. Treatment and prognosis? [If pt is disorientated in time and space amnesia]
 MOI: a) Dx: Mild Contusion- Frontal lobe predominantly right sided
- Detected in blood, ceruloplasmin level and copper level b) Topical d(x): precentral gyrus, corona radiate, internal capsule (R side post. limb
- Increased level of copper in urine ant 2/3) + vestibulocerebellar tract
 Ultrasound – find hepatomegaly
 Patients with less than 45 dise… should be excluded from this disease 2. Additional methods of investigation?
CT, Ultrasound examination, Lumbar puncture (test the CSF)
Treatment:
a. Decreased copper diet 3.Treatment?
b. Hepatosplenic transplant  Antiemetic: Metoclopramide (if nausea presents)
c. Zinc acetate  Vasoactive agents: Cyticholine
d. Chelating agent  Symptomatic treatment: Neurosurgery
 Mannitol, Tranquilizer, Domperidone
 Bed rest (2w)
 Anticonvulsant for prevention
CASE 19: A teen of 18 years old was hit to his head with a heavy object after which he lost 3.Treatment?
his consciousness for a period of several seconds. After gaining consciousness he felt an  Neurosurgical treatment (immediately)
intense headache accompanied by nausea and one vomiting episode. Within 15 minutes  Mannitol
his consciousness level gradually decreased. An ambulance urgently admitted him to a  Carbamazepine
 Valproate acid
hospital.
 Lamotrigine
Upon neurological examination: stuporous state of consciousness, neck muscles
stiffness, positive Lassegue sign, active movements appear in his right extremities in
response to painful stimuli; such response is absent in his left extremities; Babinsky sign is
What is lucid period:
positive on both sides.
In emergency medicine, a lucid interval is a temporary improvement (patient feels
Common blood test and biochemical blood analysis: no changes.
normal) in a patient's condition after a traumatic brain injury, after which the condition
ECG: sinus rhythm, no signs of focal myocardial ischemia.
deteriorates. A lucid interval is especially indicative of an epidural hematoma. 
On CT scan the following changes (see pic.):
General tonic-clonic seizure
- Look at the time (duration)
- Turn patient to the side to prevent aspiration
- Don’t put anything to mouth
- Give drug: diazepam (1m), lorazepam (depression of respiration centre is not
so great)
- After seizure, don’t give diazepam
- NaCl injection for relatives
- Pseudoepileptic seizures – give injection of NaCl

Status epilepticus
- Time – 30 mins (in real life – 5 mins. >5 mins call ambulance)
- Classical borders
1. Neurological syndromes and topical diagnosis? - Treatment: 3 stages
 Central tetraparesis (due to brain edema  ICP  whe) o First 30 mins
 Left side hemiplegia o 30 – 90 mins
[If there is no pain sensation in the left it means  plegia (paralysis)] o resistance status epilepticus - > 1 h. 30 min.
 Meningeal syndrome  due to his stiff neck - brain cells usually die
- vegetative status
Topical disnosis: - cytotoxic edema: abnormal discharges = abnormal
 Above dura mater, parietal lobe electrolytes level
 Corona radiate, internal capsule, precentral gyrus ( R side hematoma, L
side brain edema) First 30 mins how to help
- diazepam (IV) (exam) : 40 mg (max per day) – depressed respi center
2.Clinical diagnosis? - Lorazepam (for life), Clinazepam (IM)
Acute epidural haematoma on the right side (trauma) (topical epidural - above - If Diazepam no effect: give Phenytoin (IV) (ICU), intubation, valproic acid
duramater ) (IV/IM), Levitiratsitam, Phenobarbital
- If persists: Midazolam, Sodium Thiopental, Intubation, narcosis
CASE 20: A female 42 years old within the last year suffers from clonic seizures which start 3.Treatment?
from her left feet and then gradually spread over the left leg and later to the hand; such  Antiepileptic (valproate, carbamazepine)
seizures last for several seconds and are not accompanied by loss of consciousness.  Surgery to remove tumor
Within the last month the frequency of such attacks increased and they took the everyday  Steroid decreased ICP
character. The patient also become bothered by bursting headaches and she noticed the
left extremities weakness which appeared and started to increase gradually. The last
attack of seizures was accompanied by loss of consciousness and involuntary urination. CASE 21: A male of 27 years old complains of headache and gait instability. First time the
gait instability was noticed two years ago, 3 months ago bursting headaches joined and
Upon neurological examination: muscle strength in the left hand is decreased to gradually become more severe, the most severe of pains is accompanied by vomiting. The
the grade 4, in leg - to the grade 2, tendon reflexes in the left extremities are increased, patient also noticed that the headache increases when he is in a lying position on his right
positive Babinsky sign on this side, pain and temperature sensation is decreased on the side.
left side of her body. The ophthalmoscopy revealed papilledema. Upon neurological examination: Spontaneous left horizontal nystagmus to the
right, diffuse muscle tone decrease, more remarkable in the right extremities,
Common blood test and biochemical blood analysis: no changes. unsteadiness in the Romberg test and when walking with swaying to the right side, goal
ECG: sinus rhythm, no signs of focal myocardial ischemia. missing and intentional tremor in the finger-nose and heel-knee tests, more prominent in
On MRI the following changes (see pic.): the right extremities.
Malignant tumor:
Common blood test and biochemical blood analysis: no changes.
because the border is not
ECG: sinus rhythm, no signs of focal myocardial ischemia.
smooth
Benign: smooth borders

Vermis is included: due to Romberg

1 Neurological syndromes and topical diagnosis?
+ve  trunccal ataxia  swaying of
 Central left sided hemiparesis,
 generalised tonic-clonic seizures (due to loss of consciousness and body to the right
involuntary urination)
 Cerebral type of hemihyposthesia (reduction in sensitivity on one side of
the body)
 Papilledema:  intracranial pressure ( hypertensive syndrome)
Topical diagnosis: Tumor in right frontal lobe, precentral and postcentral
gyrus

MOI: MRI (contract enhancement) , CT

How to help the patient?
Neurosurgery
Treponation
Histology to find out the type of tumor: Malignant? Benign?
To know if its benign/malignant without MRI
See how long and how fast it spreads 1. Neurological syndromes and topical
2.Clinical diagnosis?
diagnosis?
 Brain tumor Malignant: quick
Benign : for years, not much difference in symptoms
  Cerebellar ataxia- static type (ipsilateral R hemisphere, vermis) - Panic disorder
 Intracranial hypertension  Should be more than 2 attack
 Accompanied with fear
 Duration 15- 20 mins
2. Clinical diagnosis?
- Cerebellar tumor  Attack should be spontaneous
3. Treatment?  Patient usually waits for new attack
a. Bed rest  Can have loss of consciousness and can do wrong behaviour
b. Methyprednisolone - Additional symptoms
c. Mannitol  Tachycardia
d. Radiotherapy/ chemotherapy  Pain in left part of chest
e. Surgical  Respiratory symptom
Common tumor in young ages: Primary (in children)  Loss of breath
Common tumor in all ages: Secondary tumor because of metastatic process  GI – constipation, diarrhea, stomachache, nausea, vomiting
 dysphagia
Main cancer type that can lead to metastatic to brain: 2. Preliminary diagnosis?
- Panic disorder
1. Melanoma: Skin cancer (MOI: just see it on the skin, then biopsy) - Generalised anxiety disorder
2. Lung (MOI: CT scan) • Patient already have anxiety in real life
3. Breast (MOI: Mammography) • Usually in the evenings without reason
4. Kidney

*Tumor from metastatic process they can imitate clinical picture ischemic stroke, because
bleeding can happen in the tumor. To differentiate: CT scan 3. Management of the patient?
MRI: Contrast imaging enhancement (because its hard to catch) - Perform ECG – cardiac complaints- patient with angina pectoris can have panic
attack
- Anxiolytic, Benzodiazepine – diazepam, clonazepam
CASE 23: A 27 year old man complains of periodic disturbances of breathing with the - Specific breathing technique – inhale deeply, 2,3,4, exhale; abdominal breathing
- antidepressants – paroxetin
following dizziness, numbness in the area of lips and in fingers of hands. The attack always
- SSRI – fluoxetine, sertraline
lasts about 15-30 minutes, after that the patient feels internal tension and the fear of the - not so good AE: dry mouth, tachycardia
new attack. - go to endocrinologist – hyperthyroidism can be trigger
The attacks appeared about three months ago and repeated about two or three - psychotherapy
times per week, mostly at night time. The father of a patient suffers from the bronchial - disease is irreversible if occurs more than 1 year
asthma, that is accompanied by the attacks of suffocation, when there is the need to call - if start early age :
an ambulance. The examination of the pulmonologist and of the cardiologist didn’t detect  Agoraphobia – fear of going out to places
any disease. There are no focal symptoms in neurological status.  Depression
 Hypochondrial features
Common blood test and biochemical blood analysis: no changes.  Patient with psychiatric predisposition
Duplex ultrasonography of carotid and vertebral arteries: no sighs of stenosis.
MRI of the brain: no focal changes (see pic.)
CASE 25: A 30 year old woman complains of attacks of pulsating headache, mostly right-
1.How can the attacks be estimated? sided. The duration of the disease is about 10 years. Headache preceded by visual
disturbances – (выпадение) of the left visual fields. Visual disturbances last about 10-15 exercise. The symptoms appeared three months ago. She also notices, that in the morning
minutes, than headache appears. The attack lasts from 3-4 hours up to 2 days and it is after rest the voice normalizes.
accompanied by nausea, vomiting, photophobia. Physical training during headache The examination showed dysphonia after the voice strain, weakness in the
increases the pain significantly. The attack can be provoked by emotional tension, by a proximal parts of the limbs (4 points), decreased tendon reflexes. Subcutaneous injection
long period of staying in a stuffy room, sometimes – by menstrual cycle. The frequency of proserin induced complete regression of neurological disturbances.
of attacks is about 1-2 per month. Mother and grandmother of the patient have similar
headaches. Neurological examination didn’t detect any disturbances. Common blood test and biochemical blood analysis: no changes.
Common blood test and biochemical blood analysis: no changes. ECG: sinus rhythm, no signs of focal myocardial ischemia.
EEG: no epileptic and other abnormal activity. Electroneurography: conduction velocity in n.ulnaris is 55 m/s and in n. medianus –
MRI of the brain: no focal changes (see pic.) 54 m/s, amplitude of muscle answers decreases essentially. By rhythmic stimulation of n.
medianus – decrement of muscle answer (see pic.)

Decrement
of amplitude
after every
stimulus
1. Clinical diagnosis?
- Migraine with aura (episodic type, <15days)
2.Treatment in the period of the attacks?
- Tryptans – GS – 5 HT, Serotonin receptors agonists,
 Zolmitriptan (headache will stop in 20 mins), sumetriptan, noratriptan
- antiemetics
- aspirin, paracetamol, NSAIDS 1. Neurological syndromes?
- Ergometerine (kofetamine,kuffein)  Peripheral tetraparesis,
 Dysphonia (decrease of voice)- Bulbar syndrome
If migraine is chronic / prophylaxis 2.Localization of lesion? (topical diagnosis)
- B-blockers  Larynx, antibodies in the post synaptic membrane of neuromuscular
- anti-depressants junction causing acetylcholine unable to bind to the receptor
- Ca2+ channel blocker 3.Preliminary clinical diagnosis?
- Antiepileptic  Myasthenia gravis (generalized)
- Dypyridamole 4.Treatment?
*No convulsants for pregnant women  Neostigmine + atropine (atropine to prevent the side effects of
neostigmine),
 Immunoglobulins
3.Prophylaxis of the attacks?  Pyridostigmine, in tablets (its for the long term therapy)
- Physical activity  Prednisolone (steroid) 1 mg to 1kg of body weight. (rarely given: cytostatic
- sleep drugs)—A/E: moon face, PUD, tachycardia, osteoporosis
CASE 26: A 36 year old woman, a teacher, complains of voice hoarseness, which CASE 27: A 25 year old man complains of weakness in right leg and of instability of gait.
appears in the end of the classes; and of weakness in limbs, especially during physical From anamnesis it is known, that at the age of 18 he had deterioration of vision in the left
eye during one week. At that time he didn't visit doctors because the vision recovered has arterial hypertension and diabetes mellitus type 2. The neurological status:
itself. Two years ago he found urinary urgency and decreased sexual potency. consciousness is clear, there are no meningeal signs. Cranial nerves are preserved.
In neurological status: horizontal nystagmus, decreased muscle strength in right leg up to Symptoms of oral automatism are detected. The strength in limbs is fine, muscle tone is
4 points, increased of knee and achilles reflexes in right leg, Babinsky sign is positive normal, tendon reflexes are symmetrical. Constant tremor of the head is observed.
there; positive Romberg test with closed eyes, decreased sensation of vibration in legs. Apparent postural tremor of hands. Romberg test is negative, coordination tests are
perfomed with a light intentional tremor. There are no sensory disturbances. Mother of a
Common blood test and biochemical blood analysis: no changes. patient also has tremor of the head.
ECG: sinus rhythm, no signs of focal myocardial ischemia.
On MRI the following changes (see pic.): Common blood test and biochemical blood analysis: no changes.
ECG: sinus rhythm, no signs of focal myocardial ischemia.
On MRI: single small (up to 5 mm) sights of high density in T2-regimen (see pic.):

1.Neurological syndromes?
- Retrobulbar neuritis, intranuclear opthalmoplegia
- Central monoparesis in rightleg
- Spinal conductive type of sensory disturbance
- Cerebellar ataxia, sensory ataxia
- MRI: demyelination – near the ventricles and corpus callosum
T1. If T2 CSF would be white 1.Neurological syndromes?
2.Localization of lesion?  Essential tremor (hyperkinesias-hypotonia)
 T10- T12 R lateral column of thoracic level  Constant tremor in head and hand
 Cerebellum lesion
 Intention tremor
 Optic n.
 Posterior column of R spinal cord (T11-T12)/ ipsilateral med
2.Preliminary clinical diagnosis?
3.Preliminary clinical diagnosis? Multiple sclerosis
 Hyperkinetic- hypotonic
 Intention/Rest tremor
4.Treatment?
- Methylprednisolone (IV)
3.Treatment and prognosis of the disease?
- pulse therapy of steroids – 100mg (IV) Everyday for 7 days
- B-blockers: Propanolol
- Asymptomatic – muscle relaxant
- Antiepileptic
- Help patient stop exacerbation
- Botulinum toxin
- M cholinoblocker: for urination
- INF B – Copaxone (1st line drugs) – patient should take forever
- monoclonal antibodies – Natalizumab (2 nd line drugs) CASE 29: A 18 year old girl complains of episodes of loss of consciousness that appear in
CASE 28: A 64 year old woman during 10 years suffers from trembling of the head (the airless rooms and in transport. Loss of consciousness follows the feeling of “faintness and
“no-no” type) and from trembling of the hands, especially when perfoming some darkness in eyes”. If the patient is able to sit or to lie at that time she can avoid loss of
operations (for example when she needs to bring the spoon to the mouth). The patient consciousness. These states disturb a patient from the age of 14, but last few months
their frequency increased to approximately one attack per week against the background short loss of consiousness. The attacks may repeat up to few tens per day. No
of the excessive emotional and physical tension (the patient combines studies in the neurological disturbances are found at the moment of examination.
institute and work). On investigation no neurological disturbances were found. Common blood test and biochemical blood analysis: no changes.
ECG: sinus rhythm, no signs of focal myocardial ischemia.
Common blood test and biochemical blood analysis: no changes.
EEG: see picture below.
ECG: sinus rhythm, no signs of focal myocardial ischemia.
1.The type of attacks?
Duplex ultrasonography of carotid and vertebral arteries: no sighs of stenosis.
- absences seizure
EEG: see picture below. (normal)
2.Preliminary clinical diagnosis?
- generalised epilepsy with loss of consciousness

3.The treatment and the prognosis?

- ethosuximide
- valproic acid

MOI
- Find out what kind of epilepsy reflexes/paresis and weakness
- Generalized – no consciousness, whole cortex is abnormal
- Partial – simple – primary – Motor (reflexes), sensory (numbness, tingling)
- secondary – autonomic (stomachache, diarrhea), psychiatric
(depression, anxiety, mood changes)
- complex

1.What is the mechanism of the attacks with loss of consciousness? Treatment

1st line – Valproic acid (1 in 1 week)
- Neurogenic/ vasovagal syncope (happens under stressful situations - Lamotrigine (1 in 2 weeks)
 adrenaline , blood pressure , Baroreceptor reflex, BP  - Levitiratsetam (for all)
 Patient have overreactivity of baroreflex ( BP drastically) -> less blood to Partial Seizure
the brain (emotional, anxiety, depression) - Carbamazepin (1 in 3 days) increase dose
2.Clinical diagnosis? - Lamotrigine
- Valproate
Neurogenic/ vasovagal syncope - Topiramide/ Phenytoin
3.Treatment? How many drugs to give patient?
- Monotherapy
a. minimal doses of B-blockers - If combine with different mechanism
b. monoamine reuptake serotonin inhibitor Pregnant women with epilepsy:
c. Psychotherapy - X valproic acid
d. Antianxiety/ relaxant - Usually lamotrigine (safest)
e. Antidepressant (last choice, as she is too young) - Tetratogenic effect (in 1st trimester)
CASE 30: Parents of a boy of 6 years old has noticed that the boy stops in his tracks for a CASE 53: A 35 year old woman complains of trembling in the fingers of hands and in the
period of few seconds. This time the boy keeps silence, his eyes are fixed, he doesn't head, that increases at excitement. The intake of alcohol reduces the trembling, but next
answer the questions and, coming back to normal state, he doesn't remember about this day after that trembling increases a little. Mother of a patient has the same symptoms
from the youth. Objectively: hand tremor at rest is minimal, but it increases in definite number of minutes the attacks usually become superseded by headache. The patient has
postures, especially when pulling the hands forward and breeding apart the fingers; also no memories of such episodes. Originally such seizures developed no more than once in
the minimal tremor of the head is observed. Tremor increases in finger-nose test. There half a year, but during the last year their frequency increased up to one per month.
are no more changes in the neurological status. Neurological status is unchanged.

Common blood test and biochemical blood analysis: no changes. Common blood test and biochemical blood analysis: no changes.
ECG: sinus rhythm, no signs of focal myocardial ischemia. ECG: sinus rhythm, no signs of focal myocardial ischemia.
MRI of the brain: no focal changes (see pic.) EEG: see picture below.

1.The type of the seizures?

1.Neurological syndromes? - Simple partial sensory seizure
Hypotonic - hyperkinetic movement disorders - Secondary tonic clonic seizures
Essential tremor 2.Preliminary clinical diagnosis?
 symmetric movement in the hands, may involve head - Tonic-clonic seizure
 autosomal-dominant inheritance
 disappears with small amount of alcohol 3.Treatment and prognosis?
- Levitiratsetam
2.Preliminary clinical diagnosis? - Carbamazepine
Essential tremor (alcohol withdrawal tremor) - Valproate
-Lamotrigine
3.Treatment and prognosis of the disease?
For tremor
• β-adrenoblockers (propranolol)
• Anti-epyleptic drugs (primidone, clonazepam)

CASE 65: Female of 65 years old developed burning pain in the right part of the thorax on
CASE 59:Male of 18 years old within the last 5 years experiences loss of consciousness the 3-d day after which she noticed vesicular eruption in this region. Within one month
episodes which start with the feeling of an unpleasant smell lasting for a number of the eruption ceased completely, but the patient is bothered by thoracic pain which
seconds after which the patient loses consciousness and develops tonic-clonic seizures of periodically increases and troubles her night sleep. The intake of non-narcotic analgetics is
his extremities accompanied by tongue biting and urinary incontinence. Lasting for a ineffective.
 Upon neurological examination: on the right side of her thorax the areas of eyelid – mydriasis, movement of the eye globe is possible only outward, no
depigmentation are found, pain hyperaesthesia at the Th5-Th10 level on the right side. movements in the right extremities, muscle tone and tendon reflexes are
Common blood test and biochemical blood analysis: no changes. increased, positive Babinsky sign.
ECG: sinus rhythm, no signs of focal myocardial ischemia.
Common blood test: no changes
ECG: sinus rhythm, no signs of focal myocardial ischemia
CT scan: no changes of brain matter’s density

In private hospital MRI of the thoracic

part of the vertebral column was done
(signs of osteochondrosis were found).

1 Neurological syndromes and topical diagnosis

- Weber’s syndrome (Oculomotor nerve palsy)
- Right side central hemiplegia
1.Neurological syndrome?
 Pain syndrome ( neuropathic pain) Topical Diagnosis: Midbrain infarction (half, left predominantly)
 Segmental radiculo type of sensory disturbances ( stripe)
2 Preliminary clinical diagnosis
2.Topical diagnosis? o Acute ischemic stroke (cardiogenic)
- Dorsal root of ganglion T5-T12 o Basilar artery (anterior vertebral)
3.Preliminary clinical diagnosis? 3 Treatment
 Postherpetic neuralgia (Neuropathic pain- that cant be relieved by analgesics) o CT Choline used in Russia, Europe and Japan
 MOI: Serologic test, Lumbar puncture (CSF) o Antihypertensive drug
o Antiaggregant, anticoagulant
4.Treatment? o Statins : Level of LDL 
 Tricyclic antidepressant (ease neuropathic pain) : Amitriptyline Cholesterol 
 Seretonin and norepinephrine reuptake inhibitor: Duloxetine (antidepressant)  Rosuvastatin
 Antiviral: acyclovir  Lovastatin
 anti-epileptic (anticonvulsants) medicines: Gabapentin, Pregabalin
 Plasters with local anesthetics like Lidocaine Every 3/6 months we should control toxic hepatitis by monitoring: AST/ALT

A male of 50 years old with a long time history of arterial hypertension and In people with Crush Syndrome, we should monitor lysis of muscle cells – rhabdomyolysis
angina pectoris during last 5 years suddenly felt weakness in the right extremities. Enzyme creatinine phosphokinase  when lysis of muscle cells
Upon examination in 2 hours after the onset: Patient is in clear ***
consciousness, no meningeal symptoms, left eye is closed, when lifting up the
A female patient of 30 years suddenly felt an intensive headache accompanied by o Jemodopon – for prevention of secondary spasm from the
vomiting and nausea, in some minutes she became unconscious. Emergency’s doctors 3rd to 5th day, which may cause secondary stroke
found her in spoor, arterial blood pressur – 180/100 mm Hg, heart rate 88 per minute, 3rd to 10th day: highest, prolonged after that
regular heart rhythm.  Surgical (for aneurysm)
Neurological status: Neck muscle rigidity, no paresis or any other neurological 1st – 2nd daysafter 21st days
disorders.  Antihypertensive drugs: to  blood pressure
Common blood test: no changes  Mannitol
ECG: sinus rhythm, no signs of focal myocardial ischemia ***
CT scan: increased density of signal in area of subarachnoid space (see pic.)
Subarachnoid hemorrhage Female of 40 years old complained of involuntary turning of the head to the right. She will
occasionally notes twitching of the head to the side. If she touches her chin with fingers, it
will provide normal position of the head. Upon neurological examination: thickening and
tension of right sternocleidomastoid muscle. There are no more changes in the
neurological status.
Common blood test and biochemical blood analysis: no changes.
ECG: sinus rhythm, no signs of focal myocardial ischemia. Duplex ultrasonography of
carotid and vertebral arteries: no signs of stenosis. On MRI of the cervical part of the
vertebral column – signs of spondylosis (see pic)

1 Neurologic
al

syndromes?
Meningeal syndrome (Proof: neck stiffness)
2 Preliminary clinical diagnosis?
 Subarachnoid haemorrhage
o Aneurysm (causes)
o Arterial hypertension
Main zones:
 Anterior communicating artery
 Posterior communicating artery
1 The type of movement disorder?
MOI: Dystonia
 CT scan (to see blood in subarachnoid space) (syndrome: Hyperkinetic (cervical dystonia – Corticolis), hypotonic syndrome 
 Substraction angiography (non-invasive) Involuntary turning of the head )
 MR-angiography -*gold standard* (non-invasive) MOI, MRI
o But a little different to detect aneurysm *Special thing* she touch her chin, it goes back to normal (in straight position)
 Lumbar puncture for a while, or women with turtle neck or women with ponytails, where she pull
3 Treatment? and it will be corrected : Correction gestures  sign of dystonia
 Bed rest for three weeks 2 Preliminary clinical diagnosis?
 Calcium channel blocker Dystonia
 3 Treatment and prognosis? o Scoliosis to the right
Botulinum toxin type A
Barbs: Clonazepam, Diazepam, BZ 3 Treatment and prognosis?
Myorelaxant (baclofen) - muscle relaxant
*** - NSAIDS – nociceptive pain – muscles etc
A male of 32 years old experienced an attack of a low back pain after lifting up heavy o 5-6 days + blockers of H2- histamine receptors to prevent gastric ulceration
things. The pain irradiated over the back-lateral surface of his right leg and did not - local anaesthetics in paravertebral points
regress. The pain increases intensively with any movement in the low back region. - steroids – Contraindicated in patients with arrhythmia
Upon neurological examination: Marked tension of back muscle, lumber region scoliosis - physical activity
curved to the right, flatness of the lumbar spine region. Movement in the low back region - psychotherapy
are markedly decreased, bending forward is impossible because of sharp pain increase. - massage / acupuncture
No paresis, no sensory disturbances and other focal neurological signs. - swimming with normal technique
IMRI of the lumbar part of the vertebral column was done (intervertebral herniation was
found) MOI:
- MRI (not all patients) – neuropathological and focal signs)
- X-rays
- Autoneuropathic examination
*if it’s neuropathy = radiculopathy

1 Neurological syndromes?
- Pain syndrome (lower back)
- muscle tension syndrome of paravertebral muscles in lumbar region
- vertebral syndrome
 Scoliosis
 Deviation of the vertebral to the right/left
 Flatness of lumbar spine
What is the normal curvatures
- kyphosis – outward curvature of thoracic and sacral region (hunching)
- lordosis – inward curvature of lumbar and cervix region

2 Preliminary clinical diagnosis?

- Acute vertebral lumbaralgia with muscle tension syndrome of paravertebral muscles in
lumbar region