Lecture on Visual Pathways For 4th Year MBBS Undergraduate Students By Prof. Dr. Hussain Ahmad Khaqan

1. Visual Pathways
Prof. Dr. Hussain Ahmad Khaqan
 MD
 FRCS(Glasgow)
 FCPS(Ophth.)
 FCPS(Vitreo Retina)
 MHPE (KMU)
 CICO(UK)
 CMT(UOL)
 Fellowship in Medical Retina (LMU, Munich)
 Fellowship in Vitreo Retinal Surgery (LMU, Munich)
 Consultant Ophthalmologist & Retinal Surgeon
Professor of Ophthalmology
Lahore General Hospital, Lahore
Ameer Ud Din Medical College, Lahore
Post Graduate Medical Institute, Lahore
Shaukat Khanum Memorial Cancer Hospital & Research Centre ,Lahore

2. CHIASMA

3. INTRODUCTION
• The chiasm permits the hemidecussation of visual
information from the temporal fields so that
information from the right VF (visual field) of both
eyes is processed in the left visual cortex and vice
versa.

4. CAUSES
Causes of chiasmal syndrome
Pituitary Adenoma
Apoplexy
Sheehan’s syndrome
Suprasellar Meningioma
Craniopharyngioma
Chiasm Optic glioma
Chiasmatic neuritis
Other Lymphoma
Metastasis
Radio necrosis
Germinoma
Cavernous haemangioma

5. CLINICAL FEATURES
• Often asymptomatic unless central (Visual acuity VA) or advanced
peripheral field loss.
• Field loss: classically bitemporal but often asymmetric and
dependent on exact site of lesion.
• Headache (usually frontal): if acute and severe, consider apoplexy.
• Hemifield slide: can occur in cases with advanced field loss and a
pre-existing phoria. The normal nasotemporal field overlap of the
two eyes is absent, leading to loss of fusion. This can cause
horizontal or vertical diplopia to be described in the absence of any
extraocular muscle misalignment.
• Post-fixation blindness: can occur during close work where an
object placed just beyond fixation (therefore in the temporal field)
may disappear.

6. ASSOCIATED FEATURESCONTINUE..
• Involvement of III, IV, VA, VB, VI, and sympathetic nerve fibres:
may result in abnormalities of pupils (including horner’s
syndrome), ocular motility, and facial sensation. Rarely see-
saw nystagmus may occur.
• Intracranial pressure (ICP): may cause nausea, vomiting,
pulsatile tinnitus, and papilloedema; hydrocephalus (blockage
of foramen of Munro from posterior chiasmal lesions) may
cause abnormal gait, urinary incontinence, drowsiness, and
Parinaud syndrome.

7. • Functioning pituitary tumours: may cause acromegaly or
gigantism (growth hormone; large hands/feet and
coarsening of features or abnormal height), Cushing’s
syndrome (adrenocorticotrophic hormone; moon face,
truncal obesity, hypertension), hyperprolactinaemia
(impotence and galactorrhoea).
ASSOCIATED FEATURESCONTINUE..

8. • Pituitary destruction causes hypopituitarism, with loss of
luteinizing hormone (LH)/follicle-stimulating hormone
(FSH) (libido, amenorrhoea; may present as primary
infertility), growth hormone (silent unless pubertal),
TSH(hypothyroidism), and adrenocorticotrophic hormone
(secondary hypoadrenalism with collapse). Hypothalamic
involvement may cause diabetes insipidus (antidiuretic
hormone; polydipsia, polyuria).
ASSOCIATED FEATURES

9. INVESTIGATIONS
• Accurate field testing and interpretation are vital.
• Urgent neuroimaging: MRI (gadolinium-enhanced) is
preferred, although CT is better at detecting bony
involvement.
• Prolactin levels.
• Consider endocrinological assessment and LP
(lumber puncture)

10. TREATMENT
Refer for appropriate treatment (e.g. to endocrinology,
neurosurgery, or often to a multi speciality pituitary team).
Treatment options for chiasmal lesions
Pituitary Medical
Surgical resection
Radiotherapy
Pituitary apoplexy Hormone replacement
Trans spheroidal decompression
Meningioma Surgical resection + radiotherapy
Craniopharyngioma Surgical resection + radiotherapy
Optic glioma Depends on whether it is benign or
malignant
Lymphocytic hypophysitis Medical

11. OPTIC RADIATIONS

12. CLINICAL FEATURES CONTINUE..
• Parietal lesions: inferior incongruous homonymous defect, usually
sparing fixation (macula fibres pass between parietal and temporal
lobes); may be associated with damage to the posterior limb of the
internal capsule (contralateral hemiparesis + hemianaesthesia),
injury to the pursuit pathways (fails to pursue to the side of the
lesion; cannot follow an optokinetic (OKN) drum rotated to the side
of the lesion), and Gerstmann syndrome (dominant parietal lobe
only).
• Temporal lesions: superior incongruous homonymous defect (‘pie in
sky’), usually sparing central vision; may be associated with
memory loss, hallucinations (olfactory, gustatory, auditory), and
receptive dysphasia.

13. • Calcarine cortex (occipital) lesions: congruous homonymous
defect; variants include sparing of the temporal crescent
(represented anteriorly), sparing of the macula (represented
posteriorly), or a congruous homonymous macular lesion
(selective injury to the occipital tip); may be associated with
visual hallucinations (usually in the hemianopic field) and
denial of blindness (Anton syndrome).
CLINICAL FEATURES

14. INVESTIGATIONS
• Urgent neuroimaging: MRI (gadolinium-enhanced) is
preferable, although CT may be adequate for many
lesions and may be advantageous in the presence of
extensive haemorrhage.

15. TREATMENT
• Refer for appropriate treatment of the underlying
cause (e.g. to stroke unit, neurosurgery, oncology).