Transcript Name the Lesion

Name the Lesion
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CASE 1
A 22-year-old man had headache and
progressively blurred vision over 3 weeks. The
patient had had relevant symptoms for 2 years.
No evidence of diabetes insipidus was found.
Examination showed impaired visual acuity in the
both eyes. Perimetric evaluation revealed
bilateral inferior temporal field defects.
Fundoscopy revealed atrophy of both optic discs.
The patient showed no adenopathy.
Case 1
Chiasmal Disorders
Case 2
R.M. was a 64-year-old right-handed woman with negative family, psychiatric,
and medical history, except for two remote events of thoracic herpes zoster
and pericarditis.
Her neurological disturbances began at age 55 with slight difficulties in object
recognition and subsequent difficulties in using them. Owing to this, she
later began to confound clothes, lost her household competence and
autonomy in doing shopping; furthermore, she had to give up working,
required supervision in household tasks and had to be accompanied out of
her home.
Five years after disease onset, R.M. showed impairment in recognizing familiar
places, reading, writing, and recognizing fingers and faces.
She was aware of her disability, and the neurological examination was
otherwise normal. She had full visual field, normal eye movements, and
good acuity.
Neuropsychological Examination 1
Spared skills
Verbal IQ
Card sorting
Verbal memory
Immed visuospatial memory
Verbal fluency
semantic
phonemic
Token Test
Praxis
Tactile recognition
Auditory recognition
Writing
Impaired Skills
Performance IQ
Design copying
Finger naming
Delayed visuospatial memory
Picture naming
Word reading
Neuropsychological Examination 2
Spared skills
Verbal IQ
Card sorting
Verbal memory
Verbal fluency
semantic
phonemic
Token Test
Praxis
Tactile recognition
Auditory recognition
Writing
Impaired Skills
Performance IQ
Design copying
Finger naming
Delayed visuospatial memory
Picture naming
Word reading
Immed visuospatial memory
Verbal fluency
semantic
Writing
Case 3
A 74-year-old male with a history of Type 2 diabetes, ischaemic heart disease,
coronary artery bypass grafting, carotid endarterectomy (left), bronchial
asthma and left hemiparesis from a previous cerebrovascular accident
presented with a loss of vision on the right side happening one morning
together with a sensation of flushing and mild giddiness.
He was admitted and assessed. He was found on initial assessment to have
right homonymous hemianopia and no other neurologic deficit apart from
the pre-existing weakness of the left upper and lower limbs. Over the next
few hours after this happened he noticed vivid images of lions and cats in
the right visual field. Over the next few days he described as seeing flock of
birds, pack of hounds, chessboards and brightly coloured scarves in the
same area.
The themes were repetitive and lasted several minutes. The patient reports that
these visual sensations tend to happen more when he is animated (talking,
laughing, etc. in the presence of company). He was sometimes annoyed by
them but was fully aware that these were not real. He was found to have a
Snellen visual acuity of 6/12 (20/40) right eye and 6/9 (20/30) left eye and
the ocular examination was otherwise normal. There was no evidence of
diabetic retinopathy.
Goldman kinetic perimetry confirmed right homonymous hemianopia with
macular sparing (Fig. 1).
Goldmann Perimetry – Case 3
MRI- Case 3
An unenhanced CT scan of his head
showed evidence of a recent left occipital
lobe ischemic infarction (in the vascular
territory of the left internal occipital artery
involving both grey and white matter) and
an old right posterior circulation infarct
affecting the occipital region sparing the
primary visual cortex.
Case 3 – Charles Bonnet Syndrome
• Theories
– “deafferentation”: lack of visual sensory input into the
cortex causing spontaneous neuronal discharge
leading to abnormal visual perceptions not unlike the
phantom limb syndrome
– “perceptual release”: normal sensory input inhibits
irrelevant impulses from the conscious perception of
images. Where there is a reduction in sensory input,
the threshold to suppress irrelevant images cannot be
achieved and previously subconscious perceptions
are ‘released’ into consciousness, resulting in a visual
hallucination
Case 4
A 4-year-old Hispanic girl came to a neighborhood community health center for her first
eye examination. She was referred by her pediatrician for vague neurologic
symptoms. Her mother stated that sometimes the child’s eyes crossed, but they
quickly returned to normal. No other problems were noted; the mother believed her
daughter saw well and had no complaints about her eyes.
The patient denied having any flashes of light or floaters and had no previous eye
trauma. She was taking no medications and had no known allergies. Her mother was
not aware of any systemic health problems or any family history of ocular or systemic
problems.
The patient’s entering uncorrected visual acuities were 20/32 in the right eye (O.D.) and
20/25 in the left eye (O.S.). Retinoscopy findings showed a mild refractive error with
vision correctable to 20/20 O.D. and O.S. Cover test results showed orthophoriaat 6
meters and 3 prism diopters of exophoria at 40 cm. Pupils were equal, round, and
reactive to light without evidence of relative afferent pupillary defect.
Extraocular muscle testing results were significant for an asymmetric, horizontal, gazeevoked nystagmus, with the left gaze worse than the right gaze. Visual fields by
confrontation were full in both eyes (OU) in all 4 quadrants O.D. and O.S. The
remainder of the exam revealed no evidence of optic nerve or retinal pathology.
After further questioning, the patient’s mother stated that on one occasion 3 weeks
earlier, the child started crying for no apparent reason. During that time, the right side
of her mouth drooped and her right eyelid closed. The mother then took the child to
her pediatrician, who ordered an electroencephalogram, the results of which were
negative.
Case 4: Large Brainstem Astrocytoma
Case 4: Gaze-Evoked Nystagmus
• GEN: rhythmic oscillation of eyes when
attempting to hold an extreme position of
fixation
• Three pathways to a saccade:
– Upper: voluntary initiation; caudate and SN
– Middle: controls saccade trajectory; SC
– Lower: initiation; burst neurons (quick);
Purkinje cells (pursuit)