| disease | Temporal Lobe Tumor |
The incidence of temporal lobe tumors ranks second among cerebral hemisphere tumors, only surpassed by the incidence of frontal lobe tumors. Common tumors include gliomas, accounting for approximately 17.96% of all intracranial gliomas, followed by meningiomas, making up about 5.42% of all intracranial meningiomas. Additionally, metastatic tumors and others frequently occur in this region. These tumors are more common in adults, with no significant gender difference. The functions of the temporal lobe are highly complex, and some areas remain incompletely understood. In the early stages of temporal lobe tumors, typical clinical symptoms are often absent, making diagnosis challenging. This is especially true for tumors located in the right temporal lobe, which mostly present with symptoms of increased intracranial pressure, while localizing symptoms and signs are rare. Consequently, this region has been clinically referred to as the "silent area" or "mute area," further complicating early diagnosis.
bubble_chart Clinical Manifestations
Temporal lobe tumors often show no obvious clinical symptoms in their early stages. As the disease progresses, temporal lobe epilepsy seizures frequently occur. Depending on the frequency of the seizures, hallucinations may accompany them. Focal seizures gradually develop into generalized tonic-clonic seizures, with visual field changes during the interictal period, such as upper quadrantanopia progressing to homonymous hemianopia, prolonged Todd's paralysis, worsening aphasia and psychiatric symptoms, and eventually leading to increased intracranial pressure. The progression of psychomotor seizures is often due to the tumor extending into the subcortical regions. The main clinical symptoms are described as follows:
2. **Sensory Aphasia** When tumors in the dominant hemisphere damage Brodmann areas 41 and 42 in the superior temporal gyrus, sensory aphasia may occur. Damage to the posterior temporal lobe can result in anomic aphasia, one of the most reliable diagnostic symptoms of temporal lobe tumors. Patients lose the ability to understand others' speech and name objects, though they retain the ability to speak. However, they often misuse words, make errors in speech, and may even exhibit logorrhea. In severe cases, their speech becomes completely incomprehensible, and they cannot understand others' language. Anomic aphasia is also a common manifestation of temporal lobe aphasia, where patients struggle to name objects and instead describe their features or uses. When the correct name is provided, patients can recognize its accuracy. Clinically, anomic aphasia is often part of the early presentation of sensory aphasia. Additionally, if the tumor extends toward the parietal or occipital lobes, symptoms such as alexia, agraphia, acalculia, and visual agnosia may appear.
3. **Epileptic Seizures** The incidence of generalized tonic-clonic seizures caused by temporal lobe tumors is second only to frontal lobe tumors. Some patients may also experience focal seizures, often due to tumor invasion into the motor area. Temporal lobe seizures are characterized by diverse auras and complex symptoms, including confusion, speech disturbances, psychomotor agitation, emotional and orientation disorders, hallucinations, illusions, and memory deficits. The fundamental symptom is memory impairment, which includes remote, recent, and immediate memory. Extensive tumor damage to brain tissue often manifests as disorientation to time, people, and places. Bilateral medial temporal lobe tumors affecting the hippocampus primarily impair immediate memory. Some temporal lobe epilepsy patients experience déjà vu (familiarity with unfamiliar places) or jamais vu (unfamiliarity with familiar places). Others may experience visual hallucinations such as metamorphopsia (distorted vision) or macropsia (enlarged vision). The auditory cortex is located in the transverse temporal gyrus, and patients with auditory hallucinations may perceive sounds as louder or softer, or hear noises like ticking clocks, songs, drums, or static. Auditory hallucinations are often accompanied by vestibular cortical vertigo and episodic tinnitus. The taste cortex is located in the lowest part of the precentral gyrus, and damage here rarely causes taste disorders, but irritation may lead to gustatory hallucinations.Temporal lobe seizures may be preceded by various auras, with olfactory auras being the most common. Patients suddenly perceive an extremely unpleasant or foul odor. This aura often occurs when medial temporal lobe tumors affect the uncus of the hippocampus, hence termed "uncinate fits." Some patients report a rising sensation from the stomach to the chest, which is also seen in temporal lobe epilepsy. However, since this aura can occur in other types of epilepsy, it lacks specific diagnostic significance.
Automatism is also a common and representative symptom of temporal lobe epilepsy, characterized by paroxysmal activities not under conscious control. Among these, behaviors such as aggression, property destruction, self-harm, impulsivity, and nudity are more frequently observed. A minority of patients often exhibit purposeless actions like chewing, smacking lips, sucking, hand groping, or head and eye twisting during seizures. In cases of deep temporal lobe tumors, paroxysmal behavioral abnormalities may occur, often accompanied by dream-like hallucinations. Patients experience a dreamy sensation, as if in a bizarre dream, frequently concurrent with visual hallucinations, resembling a return to childhood or episodes of terror.
4. Psychiatric Symptoms Psychiatric disorders are also common symptoms of temporal lobe tumors, second only to frontal lobe tumors. The main symptoms include personality changes, emotional abnormalities (such as anxiety, depression, panic, anger), paranoia-like symptoms, memory impairment, mental sluggishness, and apathy. Psychiatric symptoms are more likely to occur in tumors that grow extensively and rapidly in the dominant hemisphere's temporal lobe.
5. Ataxia The posterior parts of the middle and inferior temporal gyri are connected to the cerebellum via the temporopontocerebellar fibers. Therefore, damage to one temporal lobe can also cause contralateral hemibody ataxia, leading to balance disorders, often causing the patient to fall toward the side opposite the lesion.
6. Pyramidal Tract Signs Tumors in the upper part of the temporal lobe can compress the lower parts of the frontal and parietal lobes, resulting in motor or sensory disturbances in the face and upper limbs. Compression of the contralateral cerebral peduncle or internal capsule can lead to ipsilateral pyramidal tract signs, causing varying degrees of hemiplegia.
7. Other Symptoms Medial temporal lobe tumors can compress the midbrain, leading to oculomotor nerve palsy. When temporal lobe tumors compress the cranial cervical sympathetic plexus, Horner's syndrome may occur. Involvement of the basal ganglia can cause contralateral limb tremors, chorea, athetosis, or paralytic tremor syndrome. Invasion of the insular lobe may result in spontaneous visceral pain, among other symptoms.
bubble_chart Auxiliary Examination
1. Skull Radiography Temporal lobe tumors, like tumors in other regions, may exhibit signs of increased intracranial pressure (such as cranial suture separation, increased convolutional markings, and changes in the sella turcica) at different stages of the disease, depending on the tumor's nature, growth rate, and location within the skull. Tumor calcification (commonly seen in oligodendrogliomas, astrocytomas, meningiomas, and ependymomas) appears in the corresponding area of the temporal lobe tumor. Localized skull destruction or hyperplasia is also often consistent with the tumor's location. The above findings on skull radiography often serve as reliable evidence for diagnosing temporal lobe tumors.
2. Ventriculography For temporal lobe tumors, ventriculography primarily determines the tumor's location, with the following characteristics:
(1) Anteroposterior view: The lateral ventricle shifts toward the unaffected side. The septum pellucidum and third ventricle curve toward the opposite side. The superolateral angle of the anterior horn becomes pointed, directed outward or superolaterally. The lateral wall of the lateral ventricle becomes concave, and its transverse diameter decreases.
(2) Lateral view: Changes in the inferior horn are prominent in both lateral and anteroposterior views. If the tumor is above the inferior horn, the horn shifts either entirely or partially. If the tumor is below the inferior horn, the horn shifts upward. If the tumor is lateral, the horn shifts medially; if medial, the horn shifts laterally. Upward displacement of the inferior horn reduces the distance between it and the ventricular body.
Depending on the tumor's location, flattening or arcuate impressions may appear on the roof or floor of the inferior horn, often accompanied by displacement and narrowing of the ventricular cavity. If the tumor protrudes into the ventricular cavity, a filling defect may appear, its shape determined by the tumor's surface morphology. The inferior horn may become slender, prone to stenosis or occlusion. If the entire inferior horn narrows, rigidity often occurs simultaneously. Tumor invasion of the ventricular wall may cause irregularity in the wall's contour. Deep-seated tumors in the medial temporal lobe may compress the posterior third ventricle, leading to dilation of the lateral and third ventricles, with minimal lateral displacement. On the lateral view, the third ventricle may show grade I displacement, the direction of which depends on the tumor's position.
(3) Cerebral Angiography For temporal lobe tumors, carotid angiography primarily localizes the tumor based on vascular displacement. The characteristics of vascular displacement for tumors in different parts of the temporal lobe are as follows:
(1) Anterior Temporal Lobe Tumors
1) Anteroposterior view: The longitudinal segment of the anterior cerebral artery shifts linearly to the opposite side, with more pronounced displacement inferiorly. The genu segment of the middle cerebral artery, along with its connected horizontal and sylvian segments, straightens and shifts superomedially. In severe cases, these three segments may form a straight line pointing superolaterally, creating a V-shape with the anterior and middle cerebral arteries. The supraclinoid segment of the internal carotid artery straightens and shifts medially, with elevated branches.
2) Lateral view: The vertical segment of the anterior cerebral artery straightens and shifts anteroinferiorly. The curvature of the genu of the corpus callosum widens. The sylvian segment of the middle cerebral artery straightens and shifts upward, possibly more than 1 cm above the tuberculum sellae line. The supraclinoid segment of the internal carotid artery straightens, elevates, and runs diagonally posterosuperiorly with the sylvian segment. The anterior part of the sylvian triangle elevates. The frontoparietal ascending artery branches straighten, separate, and may also shift upward. The carotid siphon may widen. The anterior choroidal artery often straightens, thickens, and shifts upward. The anterior segment of the basal vein may shift upward and medially.
(2) Middle Temporal Lobe Tumors
1) Anteroposterior view: The longitudinal segment of the anterior cerebral artery shifts linearly to the opposite side, with varying degrees of displacement, sometimes mild. The genu segment of the middle cerebral artery straightens and shifts superomedially. Mild cases may only be detectable by comparison with the opposite side, while severe cases may show the horizontal and sylvian segments forming a straight line extending superolaterally from the internal carotid artery branches, creating a V-shape with the anterior cerebral artery. In extreme cases, it may form a convex arc superomedially. The supraclinoid segment of the internal carotid artery straightens, elongates, and shifts medially, with elevated branches.
2) Lateral view: The siphon curve is widened, and may even cause the supraclinoid segment to rise vertically in a straight line. The middle segment of the middle cerebral artery in the sylvian fissure is noticeably displaced upward. The sylvian triangle is elevated. The horizontal segment of the middle cerebral artery (M1) may be elevated and straightened, forming a straight line with the internal carotid artery as it rises vertically, while the sylvian segment connected to it abruptly turns backward at a right angle and runs horizontally. The upward displacement of the middle cerebral artery is quite pronounced, reaching the plane of the pericallosal or marginal artery. Sometimes, partial occlusion of the vessel may occur due to tumor compression. The frontoparietal ascending artery may also be displaced upward. The anterior choroidal artery becomes straightened, thickened, and displaced medially and upward. If the tumor invades the uncus or its vicinity, the anterior choroidal artery may bulge upward in an arc shape. The basal vein is displaced medially and upward. The internal cerebral vein is displaced to the contralateral side.
(3) Posterior temporal lobe tumors
1) Anteroposterior view: The longitudinal segment of the anterior cerebral artery appears straight and shifts to the contralateral side, sometimes with mild displacement. The branches of the sylvian fissure artery shift medially, and the sylvian point moves inward and upward. The genu segment of the middle cerebral artery usually remains unchanged unless the tumor involves the mid-temporal lobe. The supraclinoid segment of the internal carotid artery and the main trunks of the anterior and middle cerebral arteries typically show no deformation or displacement.
2) Lateral view: The convexity branches of the middle cerebral artery (M4, M5) are elevated, rising more than 1 cm above the clinoid line and may exhibit an upward arcuate bulge. The sylvian point is raised. If the tumor is near the temporal lobe surface, the angular artery and posterior temporal artery and their branches may become straightened and separated. The curvature of the pericallosal artery may increase. The frontoparietal ascending artery is compressed anteriorly. The choroidal artery becomes tortuous due to compression, and its posterior segment may shift downward due to hippocampal herniation. The main trunk of the internal carotid artery and the anterior cerebral artery usually show no significant changes. The basilar artery shifts medially and upward or may also shift downward. The internal cerebral vein shifts to the contralateral side.
(4) Deep temporal lobe tumors
1) Anteroposterior view: Vessels usually show no significant changes.
2) Lateral view: The middle cerebral artery shows slight upward displacement. The anterior choroidal artery may be elevated and deformed, with increased curvature and medial displacement. The posterior cerebral artery may shift downward and form an arcuate downward bulge. The basal vein may become angulated or twisted.
4. Electroencephalography (EEG) In EEG examinations of temporal lobe tumors, the detection rate of focal delta waves is very high, exceeding 90%. The delta waves are slow (0.5–2 Hz) and persistent. Background alpha waves are often abnormal. The EEG characteristics of tumors in different parts of the temporal lobe are as follows:
(1) Anterior temporal tumors: Polymorphic delta waves are relatively localized to the anterior temporal leads. Background alpha waves are generally unaffected. The detection rate of spike waves is higher. In the early stages, differentiation from frontotemporal tumors is difficult because both can cause EEG changes in the lateral frontal, prefrontal, and inferior parietal regions: ① Slow waves in frontotemporal tumors mainly appear in the lateral frontal, prefrontal, and anterior temporal regions, sometimes extending to the posterior frontal and parietal regions. ② Slow waves in anterior temporal tumors are primarily in the anterior temporal region, possibly spreading to the posterior temporal, prefrontal, and lateral frontal areas. ③ Lazy waves (unilateral weakening of alpha or fast waves, or slowing of alpha frequency) are more pronounced around the tumor.
(2) Posterior temporal tumors: Polymorphic delta waves mainly appear in the posterior and anterior temporal regions, possibly extending to the inferior parietal, parietal, and occipital regions. Around the tumor, there is a reduction in fast waves and the presence of theta waves. The background alpha waves on the affected side often show rhythm disturbances, slowed frequency, reduced amplitude, or disappearance, which can help differentiate them from anterior temporal tumors.
(3) Temporo-parieto-occipital tumors: Prominent delta waves may appear in the posterior temporal, inferior parietal, parietal, and occipital regions, but are usually most pronounced in the inferior parietal area. Bilateral, especially ipsilateral, alpha waves show significant disturbances mixed with scattered delta and theta waves.
5. Cerebral ultrasonography Ultrasonography for temporal lobe tumors has the highest localization positivity rate. In addition to tumor waves, midline shift to the contralateral side is most evident. In cases of ventricular enlargement or hydrocephalus, the amplitude of the lateral ventricular wave increases, and the distance between the lateral ventricular wave and the midline wave widens.
6. Isotope brain scanning Isotope scanning of temporal lobe tumors shows varying manifestations depending on the tumor’s nature, location, size, and blood supply. Generally, the scanning positivity rate for temporal lobe tumors is high.
7. Brain CT Examination CT diagnosis of intracranial tumors is primarily based on changes in the density of tumor tissue and the compression or displacement of the ventricular system caused by the tumor. Some tumors exhibit high density and appear clearly on CT images; others show distinct contrast due to calcification deposits. Certain tumors may display uniform or non-uniform low-density areas due to necrosis of the tumor tissue or surrounding edema. Temporal lobe tumors are mostly gliomas and meningiomas, which often appear as high-density areas on CT scans. A small number of tumors may exhibit calcification, cystic changes, necrosis, or edema, resulting in varying density patterns. The lateral and third ventricles are commonly observed to be compressed, deformed, or displaced.
Temporal lobe tumors, like frontal lobe tumors, progress relatively slowly. Clinically, they rarely present with typical symptoms. As the disease progresses, seizures may occur only when the tumor grows to a considerable size, accompanied by various hallucinations, psychiatric symptoms, visual field changes, and eventually symptoms of increased intracranial pressure. Temporal lobe tumors often need to be differentiated from the following temporal lobe diseases.
(1) Temporal lobe abscess Most temporal lobe abscesses are secondary to extracranial bacterial infections, with otogenic brain abscesses secondary to chronic suppurative otitis media or mastoiditis being the most common, followed by abscesses caused by traumatic or hematogenous infections. The clinical manifestations of temporal lobe abscesses, especially chronic ones, are very similar to those of temporal lobe tumors and can sometimes be difficult to distinguish. However, the clinical symptoms of brain abscesses, particularly systemic infection symptoms, mostly occur in the early stages. Most patients have an infection focus or recent infection history, often with bradycardia. Although body temperature may sometimes rise, it is mostly normal. Blood tests may show elevated white blood cell counts and erythrocyte sedimentation rate (ESR), and cerebrospinal fluid protein levels are often more significantly elevated than white blood cell counts. Brain ultrasound may reveal midline shift and abscess waves. Cerebral angiography shows characteristic features, and CT scans can display well-defined low-density areas. Detailed history-taking and comprehensive examinations make it easier to differentiate from tumors. For a few difficult cases, surgical exploration may be necessary for a definitive diagnosis.
(2) Subdural hematoma Temporal lobe subdural hematomas are not uncommon clinically, second only to frontal lobe hematomas. They can occur at any age and often have a clear history of trauma. Clinical symptoms typically appear more than three weeks after the injury and resemble those of convexity temporal lobe tumors. Particularly, subdural hematomas with mild trauma, no loss of consciousness at the time of injury, and a long duration can be difficult to distinguish from tumors. Diagnostic aids such as brain ultrasound, isotope brain scanning, and brain CT can help, especially cerebral angiography, which can confirm the diagnosis by revealing a spindle-shaped avascular area in the anteroposterior view.
(3) Cerebrovascular accident and hypertensive encephalopathy Some temporal lobe tumors, especially glioblastoma multiforme and metastatic tumors, can cause intratumoral hemorrhage, necrosis, or cystic changes, leading to sudden unconsciousness resembling apoplexy. This is particularly likely to be misdiagnosed as a cerebrovascular accident in patients with hypertension or arteriosclerosis, overlooking the possibility of an intracranial tumor. However, compared to cerebrovascular accidents, the clinical progression is relatively slower, and most patients exhibit symptoms of increased intracranial pressure with gradual worsening. Additionally, severe hypertension can cause acute cerebral edema, presenting with severe headache, vomiting, papilledema, visual impairment, and various focal neurological symptoms, necessitating differentiation from intracranial tumors, especially temporal lobe tumors. However, the onset is generally acute, with abnormally high blood pressure or concurrent cardiovascular or renal diseases. Fundoscopic examination may reveal narrowed arterioles, hemorrhages, or exudates. Symptoms often improve with antihypertensive and dehydration treatments, aiding in differential diagnosis. For challenging cases, cerebral angiography and CT scans can help confirm the diagnosis.
(IV) Sphenoid Ridge Tumors The most common tumors in the sphenoid ridge region are meningiomas. Based on their location, they are divided into three parts: the outer third, middle third, and inner third of the sphenoid ridge. The clinical manifestations of sphenoid ridge tumors vary depending on their location. Tumors in the **outer third** often present with ipsilateral temporal bone protrusion accompanied by exophthalmos, ipsilateral central deviation of the mouth, and epileptic seizures (primarily temporal lobe epilepsy and focal seizures). Symptoms of increased intracranial pressure usually appear in the late stage (third stage). Tumors in the **inner third** manifest as ipsilateral optic nerve atrophy and contralateral optic disc edema (Foster-Kennedy syndrome), anosmia, nasal hemianopia in the affected eye, and enlargement of the central scotoma. Due to involvement of the superior orbital fissure and cavernous sinus, orbital apex syndrome may occur, with a few cases exhibiting exophthalmos. Tumors in the **middle third**, depending on their growth direction, may exhibit some features of both inner and outer third tumors. Middle third tumors are the most common. When the tumor is large, it can compress the temporal pole and affect the frontal pole, leading to corresponding focal signs such as contralateral central deviation of the mouth or psychiatric symptoms. Plain skull X-rays may reveal bone destruction or hyperplasia in the corresponding area. Both cerebral angiography and CT scans show characteristic changes, making it easy to differentiate from temporal lobe tumors.
(V) Middle Cranial Fossa Tumors The most common tumor in this area is meningioma. Early clinical symptoms manifest as trigeminal nerve irritation and damage, with some patients showing decreased sensation on the affected side of the face and trigeminal neuralgia. Impaired eye movement on the affected side may lead to diplopia, ptosis, and mydriasis. When the optic nerve or optic tract is involved, symptoms such as decreased vision, primary optic atrophy, and homonymous hemianopia may occur. In advanced stages, the tumor may compress the medial temporal lobe, causing olfactory hallucinations and uncinate fits. Skull base imaging may reveal bone destruction or hyperplasia in the middle cranial fossa, enlargement of the foramen ovale and spinous foramen, and possible destruction of the petrous bone and sphenoid bone. Cerebral angiography shows significant dilation of the internal carotid siphon segment, elevation of the middle cerebral artery, and pathological vascularization of the tumor in the middle cranial fossa, making it relatively easy to differentiate from temporal lobe tumors.
(VI) Thalamic Tumors The most common tumors in this area are gliomas. Clinical symptoms are complex, with the most prominent being the thalamic (Dèjerine-Roussy) syndrome, which includes contralateral hemisensory impairment (especially deep sensory impairment), mild contralateral limb paresis, contralateral spontaneous pain, ipsilateral limb ataxia, and choreoathetotic movements in the affected limbs. Thalamic tumors typically have an insidious onset. When the tumor grows inward, psychiatric symptoms become more pronounced; downward extension to the hypothalamus may cause endocrine symptoms; lateral extension affecting the internal capsule may result in "two deficits" (hemiparesis and hemisensory impairment) or "three deficits" (the above plus homonymous hemianopia), and occasionally pyramidal tract involvement may occur. Extension to the thalamic occipital region may lead to contralateral homonymous hemianopia and involvement of the quadrigeminal body, manifesting as upward gaze palsy, anisocoria, tinnitus, and hearing impairment. In summary, for patients with increased intracranial pressure presenting with "two deficits" or "three deficits," psychiatric symptoms, or basal ganglia symptoms, thalamic tumor should be considered first. Further differentiation from temporal lobe tumors can be achieved through EEG, isotope scanning, ventriculography, or CT scans.
