The diagnosis of craniosynostosis includes localization and qualitative diagnosis. Different parts of craniosynostosis cause functional changes in the corresponding parts, and there is a certain correspondence between function and anatomy. Through the spatial correspondence and temporal evolution of specific functional damage and anatomical parts, combined with other clinical manifestations to infer the site of lesion invasion and expansion, which is the main content of localization diagnosis.
I. Frontal lobe lesion
The main function of frontal lobe is to control random movement, language, emotion and intelligence, and is related to visceral activity and ataxic movement.
Anterior frontal lobe
Mental, emotional, personality, behavioral and intellectual disorders.
Posterior frontal lobe (precentral gyrus)
Stimulation symptoms are d-epileptic seizures and destructive lesions causing contralateral hemiparesis.
Base of frontal lobe
Stimulation symptoms are intermittent respiration, elevated blood pressure and other vegetative dysfunctions, and destructive lesions causing psychiatric disorders.
Cynical speech center (posterior inferior frontal gyrus)
Lesions manifesting as motor aphasia.
Writing center (posterior middle frontal gyrus)
lesions manifesting as aphasia.
eye gaze center (posterior middle frontal gyrus anterior to writing center)
irritative lesions causing isotropic gaze to the healthy side in both eyes and destructive lesions causing isotropic gaze to the diseased side.
Urinary center (frontal middle gyrus)
Damage is manifested by urinary incontinence.
In addition to dementia, severe frontal lobe damage can affect the basal ganglia and cerebellum, causing pseudoparkinson’s disease and pseudocerebellar signs.
Temporal lobe lesions
The main function of the temporal lobe is auditory function.
Transverse temporal gyrus
Irritative lesions manifest as tinnitus and phantom hearing, and destructive lesions as hearing loss and sound localization disorders.
Anterior superior temporal gyrus
lesions cause loss of musicality and lesions of the posterior superior temporal gyrus (auditory center) cause sensory aphasia.
Middle temporal gyrus and inferior temporal gyrus lesions
Lesions in the middle temporal gyrus and the inferior temporal gyrus cause contralateral trunk ataxia, and lesions in the deeper part of the gyrus combine with a deficit in the ipsilateral superior 1/4 quadrant.
Medial temporal lobe lesions
Presenting with temporal lobe d-epilepsy, hook gyrus seizures, and destructive lesions presenting with memory impairment.
Extensive temporal lobe damage
It manifests as personality, behavioral, emotional and consciousness changes, memory impairment, reverse amnesia and compound hallucinatory hallucinations.
C. Parietal lobe lesions
The function of the parietal lobe overlaps with adjacent structures.
Anterior parietal lobe (postcentral gyrus)
The stimulus symptoms are contralateral limited sensory d-epilepsy and sensory abnormalities, and the destructive lesion causes hemianesthesia of the contralateral hemiplegia.
The supramarginal and angular gyri together with the superior temporal lobe
associated with speech.
The superior parietal lobule
Loss of cortical sensation such as solid perception, two-point discrimination and stereoacuity.
Inferior parietal lobule (main side)
Loss of use, writing, reading, etc.
Occipital lobe lesions
The main function of the occipital lobe is visual function.
Visual hallucinations (such as amorphous flashes or colors)
often suggest occipital lobe lesions.
Destructive lesions
It is manifested as isotropic hemianopia with “macular avoidance” (i.e., preservation of the central visual field of the macula on both sides).
Damage to both occipital lobe visual cortex
Causes cortical blindness and blindness, but pupil response to light is present.
Posterior cingulate gyrus lesion
Causes psychogenic visual impairment, manifested by distortion or loss of recognition of visual objects, and the patient is blind but denies it himself (Anton’s sign).
V. Corpus callosum lesion
The corpus callosum is a fiber connecting the neocortex of both cerebral hemispheres, it is the corpus callosum knee, body and pressure in order from anterior to posterior.
Knee
Upper limb disuse.
Somatic
The anterior 1/3 of the lesion shows aphasia and facial palsy; the middle 1/3 of the damage shows hemiplegia and pseudobulbar palsy.
Compression
Lower extremity disuse and isotropic hemianopia.
Extensive damage to the corpus callosum
causing symptoms such as mental apathy, drowsiness and lack of desire, and memory impairment.
Sixth, hemiaxial center lesion
The centrum semiovale refers to the large white matter fibers between the cerebral cortex and the basal ganglia and internal capsule.
Anterior
Contralateral limb monoplegia and motor aphasia.
Middle
Contralateral cortical sensory deficits, distal over proximal.
Posterior
Contralateral ipsilateral hemianopia and hearing impairment.
VII. Basal ganglia and internal capsule lesions
The basal ganglia is a group of neuronal nuclei under the cerebral cortex, which includes the nucleus pallidus (including the pallidum and the nucleus accumbens), the caudate nucleus, the nucleus pallidus, and the amygdala.
The internal capsule is located between the nucleus pulposus, the caudate nucleus and the thalamus, and is a necessary route for the important nerve bundles that connect the cerebral cortex with the lower centers.
The internal capsule can be divided into three parts: the frontal part is called the anterior limb, which is between the nucleus pulposus and the caudate nucleus; the occipital part is called the posterior limb, which is between the thalamus and the nucleus pulposus; and the confluence of the two parts is the geniculate part.
The striatum (including the nucleus accumbens and the caudate nucleus)
tardive dyskinesia (chorea), resting tremor (Parkinson’s syndrome).
Internal capsule
Forelimb
There is a frontal bridge bundle passing through it, which manifests as bilateral frontal ataxia when damaged
Knee
Has cortical brainstem tracts passing through it and presents with contralateral central facial tongue palsy when damaged
Hind limbs
The corticospinal tract, the thalamocortical tract, and the visual and auditory radiating fibers pass through from anterior to posterior. The damage causes contralateral limb hemiparesis, contralateral hemianesthesia, hemianopsia and auditory impairment, respectively.
VIII. Mesencephalic lesions
The mesencephalon is located above the midbrain. It is divided into thalamic part, thalamic base and subthalamic part in terms of function and occurrence.
The thalamic part is thalamus, superior thalamus and posterior thalamus. The thalamus is the subcortical center of sensation, and the superior thalamus is associated with the regulation of biological circadian rhythms. The lower thalamus is associated with visceral and metabolic activity.
Thalamus
Superior thalamus
Lesions involving the pineal gland present with precocious puberty and enuresis. Tumors of the pineal region are common.
Posterior thalamus
Contralateral isotropic hemianopia with involvement of the lateral geniculate body and hearing loss with involvement of the medial geniculate body.
Thalamus
Irritative symptoms cause contralateral hemithoracic thalamic pain, destructive symptoms are contralateral hemithoracic profound and superficial sensory deficits, and can also cause ataxia, chorea, hyperactivity and thalamic hand.
Base of the thalamus
Involvement of Luys body causes contralateral throwing disorder.
Subthalamic
Mainly manifests as endocrine and metabolic disorders and vegetative dysfunction.
Syndromes associated with the thalamus and hypothalamus
Ankylogic mutism
Damage to the reticular formation of the hypothalamus.
Mesencephalic epilepsy
Traumatic brain injury, third ventricular tumor and thalamic tumor can cause it, manifesting as symptoms of vegetative nervous system seizures: facial flushing, profuse sweating, etc.
IX. Brainstem lesions
The brainstem is divided into three parts: midbrain, pons and medulla oblongata. The motor nuclei are located in the anterior part of the brainstem, and the sensory nuclei are located in the posterior part.
The nuclei of the brainstem are arranged in order of function from the inside out: somatic motor, visceral motor, visceral sensory, and somatic sensory. Many very important vital centers (cardiovascular center, respiratory center, etc.) are located in the brainstem.
Midbrain
Ventral part of the midbrain
Weber’s syndrome is characterized by damage to the ipsilateral motoneuron or nucleus accumbens, resulting in oculomotor paralysis, combined with involvement of the ipsilateral cerebral peduncle resulting in contralateral hemiparesis.
Midbrain periaqueductal
Benedikt’s syndrome presents with ipsilateral oculomotor palsy due to damage to the ipsilateral oculomotor nerve and ipsilateral red nucleus plus contralateral limb hyperactivity, such as chorea, tremor and tardive dyskinesia.
Tetrahymena superior colliculus
Parinaud syndrome presents with impaired conjugate eye movements and inability to gaze upward. It is seen in lesions of the pineal region.
Extensive midbrain lesions present with coma, decerebrate rigidity, and tetraplegia.
Cerebral bridge
Lower ventral part of the cerebral bridge
Foville’s syndrome presenting with ipsilateral ocular gaze palsy or with facial or adductor nerve palsy plus contralateral hemiparesis.
Millard-Gubler syndrome presents with ipsilateral spreading nerve or/and facial nerve palsy plus contralateral limb hemiparesis.
Inferior pontine segment
Raymond-Cestan syndrome (pontocerebellar syndrome)
Ipsilateral cerebellar ataxia and contralateral hemianesthesia.
Lateral part of the pontocerebellum
Pontocerebellar horn syndrome initially presents with involvement of the VIII cranial nerve, followed by V, VI, VII, IX, X, D, and Ⅻ, mostly in the form of auditory neuroma and cholesteatoma.
Extensive cerebral bridge lesions
It is characterized by coma, bilateral pupil narrowing like a pinpoint, and tetraplegia.
Medulla oblongata
Ventral part of the superior medulla lingualis cross paresis.
Dorsolateral superior segment Dorsal medulla oblongata syndrome (Wallenberg’s syndrome) presents with crossed sensory deficits and ipsilateral cerebellar ataxia, ipsilateral bulbar palsy, ipsilateral Horner’s sign (Horner’s sign) and vertigo, nystagmus.
Upper central segment Damage in this area depends on the damaged cranial nerve nuclei and can cause pre olivopontine syndrome (Jackson’s syndrome), which manifests as ipsilateral lingual palsy and contralateral hemiparesis.
Denervation Tonic Tonic posture with continuous tension of the extensor muscles of the head, extremities and trunk of the whole body range. Extensive damage to the medulla oblongata mostly manifests as acute bulbar palsy and respiratory and circulatory failure leading to death.
X. Skull base lesions
Anterior cranial fossa
Forster-Kennedy syndrome (Forster-Kennedy syndrome)
It is characterized by ipsilateral optic nerve atrophy and contralateral optic nerve papilla edema with ipsilateral olfactory loss. It is most often seen in meningiomas of the olfactory sulcus that are confined to one side.
Middle cranial fossa
Optic cross syndrome
Bilateral temporal hemianopia with pituitary endocrine disorder, with optic nerve atrophy and pterygoid saddle changes. It is a typical clinical symptom of pituitary adenoma growing suprasellarly.
Supraorbital fissure and orbital apical lesions
Many posterior orbital and optic foramen tumors can cause well-defined syndromes.
Orbital apical syndrome (Rollel syndrome)
Involvement of branches 1 and 2 of III, IV and V and VI cranial nerve, manifested by optic nerve atrophy or edema, ptosis, ocular fixation, loss of corneal reflex, and sensory disturbance in the ophthalmic and maxillary nerve distribution areas.
Supraorbital fissure syndrome (Rochon-Duvigneaud syndrome)
Same as above, except no optic nerve changes.
Spongy sinus syndrome
The lesions involve the III, IV, V and VI cranial nerves, with fixation of the eye, dilated pupils, and diminished corneal reflexes, and may be combined with proptosis and ocular venous reflux disorders. Lesions in the cavernous sinus area are often caused by thrombophlebitis, aneurysms and intra-saddle tumors involving the cavernous sinus.
Rock lesions
Rock-tip syndrome (Gradenigo syndrome)
Ipsilateral trigeminal nerve involvement causes facial pain or numbness, and abducens nerve involvement causes inward slanting of the eye and diplopia. The apical lesion is often due to the spread of papillary inflammation and the erosion of malignant tumors in the nasopharynx or sinuses along the fissure at the base of the skull.
Paracentral trigeminal nerve syndrome (Raeder’s syndrome)
The lesion is located near the semilunar segment of the trigeminal nerve in the anterior segment of the rock bone, with trigeminal nerve involvement causing facial pain and carotid sympathetic plexus involvement causing ipsilateral Horner’s sign.
Pterygopalatine syndrome (Jacob’s syndrome)
Pterygoid junction lesion causes III, IV, V and VI cranial nerve palsy, manifested by ipsilateral ophthalmic muscle paralysis and trigeminal nerve sensory disorder, such as involvement of the optic nerve causing visual impairment.
Posterior cranial fossa
Internal auditory canal syndrome
The lesion starts in the internal auditory canal with peripheral paralysis of the ipsilateral lateral nerve and involvement of the ipsilateral auditory nerve causing tinnitus, deafness, nystagmus and balance disorders.
Pontocerebellar horn lesion
The pontocerebellar horn (cerebellar-pontine pool) is the triangular space between the lateral aspect of the cerebellum and the pontine bridge and the inner 1/3 of the petrous crest.
It is ventral to the trigeminal nerve from the cerebral bridge to the rocky tip, inferior to the glossopharyngeal nerve, with the abducens nerve at the medial edge of the triangle, and the facial and local auditory nerves crossing this triangle toward the inner ear gate.
Lesions in this region often cause manifestations of involvement of the corresponding cranial nerves, which are commonly seen in auditory neuromas and meningiomas.
Jugular foramen area
Jugular foramen syndrome (Vernet’s syndrome)
The medial part of the jugular foramen is the area where the Ⅸ, X and D cranial nerves pass through.
Craniospinal canal syndrome
Lesions near the greater occipital foramen often invade the posterior cranial fossa and the higher spinal canal in both intervals, successively involving structures such as the cerebellum, medulla oblongata, posterior group of cranial nerves and upper cervical medulla.
XI. Cerebellar lesions
Cerebellar hemispheres
Ipsilateral limb ataxia, nystagmus, poor distance discrimination, and rotational disorders. Positive finger-nose and heel-knee-shin tests, decreased muscle tone in the ipsilateral hemithorax.
Earthworm
Trunk ataxia, cerebellar tyrannical speech, rarely reduced muscle tone and limb abnormalities.
Dentate nucleus
Hypermobility, myoclonus.
Cerebellar peduncle
Lesions of the superior cerebellar peduncle (binding arm) cause ipsilateral cerebellar ataxia, lesions of the contralateral red nucleus cause involuntary movements and head deviation to the diseased side; lesions of the middle cerebellar peduncle (pontine arm) show frontal ataxia; lesions of the inferior cerebellar peduncle (cordus) cause ipsilateral cerebellar ataxia, balance disorders, nystagmus and dysgraphia.