Patient's Name: Yuri Alexeivich Shur

Age: 71
Sex: Male
Address: Moscow
Status: Married
Date of Admission: 17 November 2008

Complaints:

Patient complained of moderate pain on the spine, originating from the level of T12-L2,
during normal physical activity. The pain radiates toward the lateral aspect of the right
thigh on several occasions and is more pronounced on walking (patient can walk up to 50
meters or 2 flight of stairs before feeling pain in the dorsal pelvic region). The pain is
relieved during rest (sitting or lying in supine position).

Furthermore, patient complained of weakness on the right leg. The onset of weakness is
sudden. The weakness is present on resting and on performing physical activity.

Anamnesis Morbi:

Around the year 1983, patient had a known case of hyperthyroidism which was
complicated with cardiomyopathy and ophthalmopathy. Painful palpitations were
marked. Surgical partial thyroidectomy was carried out, and patient received antithyroid
medications. Postsurgical thyroid and cardiovascular status was satisfactory.
Exophthalmos of the right eye was marked as well with mild left eye visual disturbances.
Radiotherapy was carried out and patient was treated with Dexazone injection.
Postradiologic therapy, patients ophthalmopathic condition was partially rectified, with
complaints limited to double vision on several ocular movements and bilateral
dysfunction in accommodation (left eye: myopic, while the right eye: hyperopic).

First signs of pain in spine were noted around the year 2000. Patient did not visit any
clinic during this time. The pain progressed from mild to severe in 2003.

In 2004, patient was diagnosed with cataract on both eyes. However, the condition of the
right eye was worse and hence, an artificial lens was implanted (in the right eye). The
progression of cataract was slower in the left eye and therefore no action was taken to the
left eye. Since then, patients ophthalmic conditions have been relatively stable without
severe or progressive changes.

Patient also experienced arrhythmia in 2004 and was admitted into a hospital. A
temporary pacemaker was used to normalize the cardiac rhythm.

During this time, patient noted mild weakness of his right legs without disturbance of
temperature or pain sensation.
The pain felt around the patients lumbar region (while walking) as well as progression
of weakness in the right leg lead to an abnormal gait several years later and this has
brought him into the clinic in November 2008.

19 November 2008, MRI scan was performed and marked the presences of microstroke
in the cortex, but details were not discussed with the patient.

Patient had surgical inguinal hernia repair done, but could not recall the details. In 1998,
patient experienced hearing loss and started using hearing aides. From the year 2000 until
now, patient has not experienced nausea, vomiting, headaches, dizziness and sleeping or
pelvic disorders.

Anamnesis Vitae:

Patient is currently 71 years old and is a pensioner.

He is an active smoker and has been smoking for approximately 40 years. Patient is only
a social drinker and only drinks on several occasions (about 100-150g of alcoholic
content).

He has no allergy to any drugs and has suffered no other severe diseases.

Physical Examinations:
Cranial nerves Examinations:

Number Cranial Nerve Results

I Olfactory N
II Optic Visual field: Right: N Left: N
Visual acuity: was not performed
Colour blindness: Absent

III Occulomotor Eyes movement:

Right eye--medial and superior gaze palsy
IV Trochlear Left eye--medial inferior oblique and superior
gaze palsy
VI Abducent Converging gaze palsy
Pupillary reflex: Absent
Nystagmus: Absent
Ptosis: Absent
 V Trigeminal Sensory function: N

Motor function:
Mandible power: N
Trimus/ Lock Jaw: N

VII Facial Mimic muscles: Normal

VIII Vestibulocochlear Hearing(with help of hearing aid): Right: N Left: N

Dizziness: Absent
Vertiligo: Absent
Nausea: Absent

IX Glossopharyngeal Swallowing: N
Symmetry of soft palate: N
X Vagus Oropharynx: was not performed

XI Accessory Shoulder muscles: N

Sternocleidomastoidius muscles: Right : N Left: N

XII Hypoglossal Protusion: N

Deviation: Absent
Fibrilation: Absent
Fasiculation: Absent

Note: N = Normal

General inspections:

On general inspections, there are absent of muscle wasting and muscle atrophy.
Fasciculation of the muscles is not seen. Mild pitting edema was noted on both legs.

Neurological Examinations:

Abbreviations:
N = Normal
(-) = Negative
(+) = Positive

Gradings for muscle power:

0 = Complete paralysis.
1 = Flicker of contraction possible.
2 = Movement is possible when gravitation is excluded.
3 = Movement is possible against gravity but not if any further resistance is added.
4 = Movement is possible against gravity and some resistance.
5 = Movement is of normal power.
Gradings for muscle reflex:
0 = No reflex.
+ = Reduced reflex
++ = Normal reflex
+++ = Exaggerated reflex
++++ = Exaggerated clonus

Gradings for sensory:

N = Normal
R = Slightly reduced
RR = Moderately reduced
RRR = Severely reduced

Upper Limbs:

Right Left
Movements
Shoulders (Abduction, Adduction, N N
Extension, Flexion, Protrusion,
Extrusion)
Arms (Flexion, Extension, Pronation, N N
Supination)
Tone
Biceps and Triceps N N
Flexor and Extensor of forearms N N
Power
Biceps 4 5
Triceps 4 5
Wrist muscles 5 5
Thumb index 5 5
Thumb V finger 5 5
Reflex
Bicep jerk ++ ++
Tricep jerk ++ ++
Brachialradial jerk ++ ++
Upper Rossolimo sign (Hoffman sign) (-) (+)
Coordination
Finger nose
- fast N N
- slow N N
- closed eyes N N
Rotation (rapid alternating movements) N N
Rebound N N
 Sensory
Pain N N
Temperature N N
Vibration N N
Propioception N N

Lower Limbs:

Right Left
Movements:
Thighs (Abduction, Adduction, RR N
Flexion, Extension)
Legs (Flexion, Extension) RR N
Foot (Flexion, Extension, Eversion, RR N
Inversion)
Tone
Quadriceps and Biceps 4 5
Flexors and Extensors of Legs 4 5
Peronius and Triceps surae 4 4
Clonus (+) (+)
Power
Hips
- Flexion 3 5
- Extension 4 4
- Abduction 4 5
- Adduction 4 5
Knees
- Flexion 3 5
- Extension 3 4
Ankle
- Plantarflexion 3 5
- Dorsiflexion 3 5
Reflex
Knee jerk +++ ++
Ankle jerk ++ ++
Babinskys sign (+) (-)
Lower Rossolimos sign WNP WNP
Coordination
Heel shin test Slow N
No tremor
Rombergs sign N - Stable with both opened and closed eyes.

Gait Shuffling gaitdragged right foot with

minimal flexion
 Sensory
Pain
- Thighs N N
- Legs R N
- Feet N N

Temperature
- Thighs N N
- Legs R N
- Feet N N
Vibration
- Knees 5.5 6.5
- Ankles 7 7
- Toe 6 7
Proprioception WNP WNP
(WNPwas not performed)

Syndrome: Stroke (lacunar infarct)

Topological Diagnosis: Lesion in the level of posterior limb of the left internal capsule
especially in the motor aspect.

Discussion
Reason for Diagnosis:

1. Patient exhibited symptoms of upper motor neuron disturbances: hyperreflexia of

the right knee tendon, presence of pathologic segmental reflexes such as
Babinskis sign in the right leg, and spastic weakness of the right leg. This
excludes the possibility of the lesion being at the level of lower motor neuron
(which is from the anterior horn motor neuron till the muscles).

2. In localizing the level of lesion, the patients ophthalmic (oculomotor and

trochlear neuropathy) symptoms seem to indicate a lesion in the brainstem, but
this may not be, due to several reasons:

a. These ophthalmic disturbances may have been caused by the destructive

changes of the past hyperthyroidism complicated with ophthalmopathy,
and the patient has already stated that the condition of his eyes has not
worsened since that time. This implies that such lesions in the brainstem-
ophthalmic region would have not progressed since the past 25 years and
therefore is not really a problem we need to focus on.

b. Even with the ophthalmic disturbances, bilateral ptosis was absent in this
patient. This is more an indicative sign of neuropathic damage rather than
damage of the central oculomotor and trochlear nucleus in the midbrain.
These damages were probably caused by fibrosis forming after the
 periorbital myxedema developed in the ophthalmopathy, which
compressed the nerves in the orbital region. This, therefore, excludes
brainstem lesion.

c. Patients upper limbs showed no signs of neurological symptoms. This

then, excludes the lesion being in any cervical and brainstem region. This
is because ipsilateral symptoms of lower motor neuron disturbances
should have been noted in the event of the former, and crossed paralysis
should be marked in the event of the latter.

3. We are left with the precentral gyri motor cortex, internal capsule and
thoracolumbar portion of spinal cord as possible candidates in localizing the
lesion. Since the patients sensory pathways both in the upper and lower limbs
seem to be in tact, we can probably exclude dorsal aspect (column and horn) of
the spinal cord or to some extent, the spinal cord itself as a possible candidate.

4. It is quite clear the next few questions pertaining to the lesion will be in the field
of the cortex. Hence:
a. Extrapyramidal symptoms were not present in the patient; hence the basal
ganglia-stiatum-thalamic complex should be intact.

b. As the patient showed no signs of optic nerve damage, we may exclude

large cerebral arteries such as middle and posterior cerebral arteries. This
indirectly excludes involvement of ischemia in the cortical region. This
further supported by the lack of cortical infarct symptoms in the patient,
such as dysphasia and parietal lobe signs.

c. Finally,the lesion would then be limited to only small arteries of the brain
which involves internal capsule.

Patient developing lacunar infarct would present 1 of 4 forms of this syndrome: Either
pure sensory, sensorimotor or mixed, ataxic hemiparesis, or the most commonpure
motor. Therefore it is only logical we make the diagnosis of pure motor lacunar infarct as
the preliminary diagnosis.

The next step is to confirm this diagnosis by MRI of the cortex. This step is important to
investigate the severity of the pathologic process of the infarct.

It is important to note that the pain is just as important a symptom of which we need to
further investigate by MRI.

Patient at this level may develop pain at the back due to a number of reasons. Pain may
be due to malignancy, active inflammatory process, degenerative bone process,
rheumatologic disorders or even malabsorption. It is important to isolate the leading
cause of pain, and to be sure that the pain is not associated with the right leg monoplegia.
Pathogenesis

It is obvious that the hyperthyroidism complicated with cardiomyopathy is the primary

factor for stroke. Increased incidence of arrhythmia predisposes the development of
thrombotic process in the ventricles which in time may risk thromboembolism of the
brain.

This is due to the irregular contractions of the heart which allow abnormal blood flow
that leads to a hypercoagulative state.

This, exacerbated with hypertension eases the cardiovascular wall damage process and
risks thrmbosis and neovascularisation. Added wear and tear effects of the blood flow and
recurrent hemmorrages, the emboli separates from the tail of thrombotic plaque and exit
the heart and into the brain.

In this patients case, the microemboli was silent and asymptomatic causing infarction at
the level of internal capsule especially in the aspect where corticospinal tract exits. The
nature of the corticospinal tract to decussate in the medulla brings about the weakness in
the contralateral side of the patient; the right leg of the patient, without sensory deficits.
 RUSSIAN FEDERATION MINISTRY OF HEALTH
STATE EDUCATIONAL BOARD ON HIGHER PROFESSIONAL EDUCATION

MOSCOW MEDICAL ACADEMY

I. M. SECHENOV

MEDICAL FACULTY
DIVISION FOR FOREIGN STUDENTS WITH
INSTRUCTIONS IN ENGLISH

DEPARTMENT OF NEUROLOGY

PATIENTS CASE REPORT

NAME: HUZAIFAH ABDUL WAHAB

GROUP: 14
TUTOR: DR. M. V. CHURYUKANOV

Moscow, 2008
 RUSSIAN FEDERATION MINISTRY OF HEALTH
STATE EDUCATIONAL BOARD ON HIGHER PROFESSIONAL EDUCATION

MOSCOW MEDICAL ACADEMY

I. M. SECHENOV

MEDICAL FACULTY
DIVISION FOR FOREIGN STUDENTS WITH
INSTRUCTIONS IN ENGLISH

DEPARTMENT OF NEUROLOGY

PATIENTS CASE REPORT

NAME: CHEE HUEY LI

GROUP: 14
TUTOR: DR. M. V. CHURYUKANOV

Moscow, 2008