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ORIGINAL ARTICLE
Year : 2023 | Volume
: 50
| Issue : 1 | Page : 88-96
Thalamus - The gateway to cerebral cortex
Radhakrishna Hari, Bimal Prasad Padhy, Mitalee Kar
Department of Neurology, Care Hospitals, Hyderabad, Telangana, India
Correspondence Address:
Radhakrishna Hari
Senior Consultant Neurologist, Care Hospitals, Nampally, Hyderabad, Telangana
India
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/jss.jss_142_21
Introduction: Thalamus is an oval mass of gray matter between the third ventricle and the internal capsule. The medial, spinal, and trigeminal lemnisci are the great ascending sensory projections from the periphery. The lateral and medial geniculate bodies transmit the visual and auditory information to the cortex. The thalamus also contains motor projections from the basal ganglia, on their way to the motor cortex and supplementary motor area. Materials and Methods: Over 2-year period from November 2015 onward, 83 patients with magnetic resonance imaging confirmed nontraumatic thalamic lesions were identified, and followed up. The patient population consisted of adults above 18 years of age. They were investigated as to the cause of the lesion and treated. Results: There were 58 male patients, 25 female patients. Stroke was the major cause while less common diseases causing thalamic lesions were demyelination, tumor, calcification, and gliosis. The lesions were more common on the left side. The extent of thalamic involvement was global (50.6%) most commonly. The next common was posteromedial affection (18.1%) and dorsal thalamus (14.5%). Corresponding motor weakness (57.8%) was the most common symptom, though other symptoms such as sensory loss (30.1%), ataxia (27.7%), memory loss (12%), and gaze paresis (30.1%) were also present. Headache (31.3%) and giddiness (24%) were less common than motor weakness. Speech disturbance was seen in 49.4% of patients. Discussion: Stroke is unilateral disease, while venous thrombosis, demyelination, tumor, metabolic diseases and infection can affect thalami bilaterally. While stroke can explain the sudden onset of sensory and motor disturbances, some features like cognitive dysfunction were difficult to explain. A transient disorientation to time can follow acute anterior thalamic lesions. Some patients had language disturbances suggesting that the language dominance can extend down up to thalamus. Chronic pain can also be due to a gliotic lesion in the thalamus. Upward gaze palsy seen in a third of our patients could be due to global thalamic or due to medial longitudinal fasciculus involvement. Two patients had visual hemineglect. Sleep disturbances could also be observed in thalamic disease. Asterixis and hemifacial spasm were not seen in our patients. Three patients with strokes had brachial onset seizures, and one patient had generalized seizures. Different types of gait disturbances were observed in thalamic disease including ataxia, astasia-abasia, and hemiparetic gait. Conclusion: The most common thalamic lesion was an ischemic stroke, followed by bleed. Global thalamic involvement was more common than other partial lesions, though posteromedial and dorsal lesions are also commonly seen. Sensorimotor dysfunction is the most common clinical presentation and less frequent presentations include aphasia, memory disturbances, behavioral, and cognitive dysfunction. Movement disorders, ataxic gait, sleep disturbances, and infrequently, seizures were seen in our series.
Keywords: Cheiro-oral syndrome, chronotaraxis, delirium, lemniscal projections, pusher syndrome, thalamic aphasia, thalamus
“Thalamus” is a Greek word which means “inner chamber.”
The main somatosensory pathway going to the thalamus consists of ventral posterior lateral (VPL) and ventral posterior medial (VPM) nuclei which transmit the medial leminiscal and spinothalamic projections from the body (VPL) and from the face and anterior head regions through trigeminothalamic connections (VPM). The projections from thalamus reach the primary somatosensory cortex on the post central gyrus. The inner aspect of the postcentral gyrus houses the secondary somesthetic region which receives nociceptive input from spinothalamic tract.[1],[2] The lateral geniculate body receives retinotopic input via the optic tract from the contralateral visual field. The optic radiation from the upper visual field goes through the temporal lobe white matter looping around the temporal horn of lateral ventricle (Meyer's loop), while the optic radiation from the lower visual field passes deep in the parietal white matter (Baum's loop).[1],[2],[3] The medial geniculate body receives tonotopically organized afferent auditory fibers from trapezoid body and inferior colliculus via the brachium. It further projects to the primary auditory cortex in the superior temporal gyrus (Transverse gyrus of Heschl).[4]
The ventral lateral (VL) thalamic nucleus is a motor nucleus, receiving fibers from the dentate nucleus of the cerebellum mainly, and a small input from the basal ganglia as well. The onward projection from the VL nucleus is to area 4 of the precentral gyrus (primary motor area). There is also a smaller projection to the premotor cortex, thus forming a motor feedback from the cerebellum and basal ganglia to the cerebral cortex.[2]
The ventral anterior (VA) nucleus is the main mode of connection with basal ganglia especially the globus pallidus interna and substantia nigra, pars reticulata. In turn, the VA projects to the premotor cortex including the supplementary motor area of the frontal lobes and are involved in the planning and initiation of movements. The centromedian nucleus of the intralaminar nuclear complex also has reciprocal connections with globus pallidus and premotor cortex and appears to function as part of the basal ganglia feedback system.[5]
Thalamic nuclei contain many inhibitory neurons (GABA-ergic and peptidergic) that can affect signal transmission through the thalamus. Many thalamic nuclei also contain the terminations of neuromodulatory projections such as serotonin or norepinephrine systems, from the brainstem nuclei. There are two basic types of inputs to the thalamus. The first of these is the input that is directly related to sensori-motor cortex. The second input is a modulatory input from cerebral cortex, ascending reticular system and from brainstem areas. These modulatory pathways effect the transmission of both facilitatory as well as inhibitory impulses.[2],[6]
Each thalamic neuron exists in one of the two basic physiological firing modes-”tonic mode (on mode)” and “burst mode (off mode).” The burst mode is peculiar to thalamus in the sense the neurons in this state have an intrinsic rhythmicity. This state is also called “oscillatory mode” and is probably responsible for the thalamus to act as an intrinsic pacemaker (responsible for the generation of the electroencephalographic rhythm), and also for the physiological transition into various phases of sleep. In tonic mode, the neurons respond like any other neuron, to depolarization and to hyperpolarization. In contrast, a thalamic neuron in the burst mode is tonically hyperpolarized. A special type of powerful low threshold (T type) calcium channels open up which result in rhythmic depolarization, producing a rhythmic high frequency burst of action potentials in the thalamic projection neurons.[6] This latter effect probably is influenced by some input from the visual cortex. The tonic mode in the lateral geniculate nucleus neurons is responsible for the relay of visual information from the retina to the visual cortex.
During burst mode, the neurons cannot communicate specific information. Most thalamic neurons are in burst mode during sleep.
With increasing knowledge of different functions of thalamic neurons, the key role of the thalamus in cognition, working memory, learning, and in decision-making is being increasingly recognized.[7],[8],[9],[10],[11]
The nontraumatic thalamic diseases can be of the following pathologies:
Vascular lesions–strokeMetabolic diseases–osmotic demyelination syndromeReversible posterior encephalopathy syndromeNondemyelinating inflammatory disease– vasculitis (e.g.,– Behcet disease), or connective disease (e.g., Sjogren syndrome)Neoplastic-Glioblastoma, metastatic depositsInfections – brain abscess, viral encephalitides (Japanese encephalitis, dengue virus), multifocal leukoencephalopathyPost infective demyelinating diseases – steroid responsiveDegenerative disease – Creutzfeldt-Jakob disease (CJD), thalamic dementia[12],[13]Calcification.Clinical features of thalamic involvement
Delirium
Delirium can be a presentation when there is an acute lesion even when small, involving the thalamus.[3],[14]
Psychiatric disorders
Right thalamic dysfunction is associated with schizophreniform disorders. Right mediodorsal and pulvinar nuclei dysfunction is probably responsible for this by disrupting the sensory processing and thalamo-prefrontal circuits, which normally mediate belief analysis.[15],[16],[17] Temporal and thalamocortical hyperconnectivity (when compared to connectivity of other subcortical structures with cerebral cortex), is also described in autism spectrum disorder (ASD) mediated by impaired balance between calcium channels and GABA receptors.[18],[19],[20]
Thalamic aphasia
The hemispheric language dominance extends down to thalamic level too, thus explaining the presence of aphasia in some thalamic stroke patients. The anterior nucleus of thalamus is a part of Papez circuit which further projects to cingulate gyrus of frontal lobe. Papez circuit is important for the registration and retrieval of short-term memory (Kirshner and Kistler).[8],[13] Patients with fluent aphasia were also described following dominant thalamic lesions.[11]
Thalamic pain, numbness, and hemisensory loss
The more common symptom of thalamic pain may start immediately or after 2–4 weeks after the insult. Some patients may complain of a distorted sense of taste.[21] Contrary to traditional teaching that organic lesions tend to overlap with normal sensation, the thalamic sensory loss may sometimes split exactly at the midline including the head. Thalamic pain can also be present when the lesion is at the parietal lobe, medial leminiscus, or dorsolateral medulla and hence, neuro-imaging is necessary for proper localization.
Isolated paresthesia confined to one side of the body, not accompanied by demonstrable sensory and/or motor deficits is a rare manifestation of a thalamic lacune.[22]
Tiny thalamic infarcts can present with variety of sensory deficits that can be difficult sometimes to diagnose clinically. (a) Isolated oral of facial sensory loss due to involvement of contralateral VPM nucleus, (b) Cheiro– oral syndrome, involving contralateral sensory deficit of fingers and hemimouth,[23] (c) Cheiro-oro-pedal syndrome, where hemimouth, fingers and foot on one side are hypoesthetic, (d) Sensory loss confined to the tip of the tongue and lower lip as was first reported in a 62-year-old man with a small hematoma in corresponding medial right thalamus. These findings indicate that central neurological involvement should not be overlooked when tiny areas are involved acutely.[24]
Movement disorders
Choreoathetosis, hemiballismus, and tremor are well described with acute thalamic lesions and sometimes with chronic lesions too.[25] Tremor in a chronic case may be mistaken for an essential tremor. “Pusher syndrome” is truncal tilt away from the side of the lesion observed in some vascular lesions of thalamus and basal ganglia. It is said that misperception of the vertical posture and truncal tilt gives rise to inappropriate corrective movements. Essential tremor can be suppressed by chronic bilateral deep brain stimulation (DBS) of the ventral intermediate nucleus of thalamus which receives the cerebellar projections from the dentate nucleus.[26],[27],[28] Bilateral high-frequency stimulation of the posterior oral ventral nucleus of the thalamus was useful in one patient with severe choreo-acanthocytosis which was refractory to medical treatment. The therapeutic effect persisted for nearly 1 year.[29] Thalamic asterixis was noticed in 11 patients of thalamic hemorrhage, by Donat.[30]
Vertical gaze palsy following acute thalamic lesions is well known, particularly affecting the upward gaze, wherein the patients tend to “peer at the tip of the nose.” The patient may complain of blurred vision, diplopia, or bitemporal visual field defects. In general, the visual symptom is associated with gait ataxia with normal motor power or hemiparesis and hemihypoesthesia.
Unilateral hemineglect is rarely observed with acute thalamic lesions, particularly with right-sided lesions.[31]
Seizures
Anterior thalamic region plays a major part in the maintenance and propagation of seizures.[32] Neuromodulation by way of DBS of the anterior thalamus is a good choice for refractory epilepsy, where resective surgery is not possible.[33],[34],[35] Rarely acute thalamic stroke can present with frequent seizures.
Sleep disturbances
There can be a complete lack of sleep, or more commonly difficulty in falling asleep, or fragmented sleep. This symptom may be seen in acute vascular illnesses, and chronic degenerative diseases also.
Materials and MethodsThe present study was conducted for nearly 2 years from the later part of 2015 prospectively recruiting only nontraumatic patients who satisfied the eligibility criteria. The study population included both inpatients and outpatients in our neurology services; only patients with proven magnetic resonance imaging (MRI) lesions were included in the study. All patients below 18 years of age, and those with genetic epilepsy syndromes were excluded from the study. Ethics committee approval was obtained and all the patients consented for inclusion in the study.
The laboratory work-up included routine blood tests, venous blood glucose-both fasting and postprandial, renal, hepatic and thyroid function tests, fasting lipid profile, serum ceruloplasmin, and arterial blood gas testing (wherever necessary). MRI brain was performed on 1.5 Tesla Siemens Magnetom Avanto (ATIN-DOT system) machine with 16 channel head coil. Images were obtained in the following sequences– Axial diffusion-weighted imaging, Apparent diffusion coefficient (ADC), fluid attenuated inversion recovery (FLAIR), susceptibility weighted imaging, T1 and T2, post contrast T1 and FLAIR, magnetic resonance (MR) venography and MR angiography of the brain in TOF sequence.
ResultsThere were a total of 83 patients enrolled in the study. Male patients were 58 in number and females were 25 in number. Six types of lesions were identified on imaging – infarcts, bleed, demyelination, gliotic area, tumor, and calcification [Figure 1] and [Figure 2]. Diabetic patients were 41 (41.9%) and 58 (69.4%) were hypertensives. Nearly 19.3% of patients had the concomitant cardiac illness. In this cohort, 4 (4.8%) had chronic kidney disease and two were on regular maintenance hemodialysis. Seventeen (20.5%) were found to be alcoholics. Two patients had obstructive sleep apnea. Imaging showed left-sided lesions more commonly.
Figure 1: Types of thalamic lesions and the number of patients with each type of lesion
Figure 2: Bar diagram showing symptom correlation with part of thalamus involvementOn symptom analysis, many patients had nonspecific symptoms in the form of headache (31.3%) and giddiness (24%). Important localizing symptoms were motor weakness (59%), slurred speech (49.4%), and sensory symptoms such as pain (31.3%). Loss of consciousness was seen in 13% of patients, in whom Glasgow Coma Score was calculated. Seizures were present in 13.3% of patients, behavioral disturbances in 6% of patients, and movement disorders in 1.2% of patients.
Neurological examination most commonly showed motor weakness in 57.8% of patients, followed by dysarthria with upper motor neuron facial involvement in 49.4% of patients. Gait abnormality was seen in 59% as a result of motor weakness and ataxia. Sensory impairment was observed in 30.1% of patients mostly involving touch and pain perception. Upward gaze restriction was seen in 30.1% of patients. Memory disturbances were observed in 12% of patients.
Most commonly, there was global involvement of the thalamus. Whenever there was partial involvement, it was the posteromedial part that was more commonly affected. The most common pathological process was infarct seen in 52 patients and bleed in 27 patients [Figure 2]. In both cases, global involvement was the most common [Table 1]. The second most common involvement was dorsal thalamus in case of infarcts and posteromedial thalamus in case of bleeds. The most common type of clinical presentation of thalamic infarcts was motor weakness and speech disturbances, followed by sensory disturbances, especially painful paresthesia. In case of thalamic bleeds, the common presentation was motor weakness and speech disturbance. Besides, a significant number of thalamic bleed patients (16 out of 27 patients) had headache as a presenting symptom. Loss of consciousness, gaze palsies, and other presentations were less common. The other types of lesions were far less common and are represented by a single case in each category in our series [Table 2].
We tried to get an insight into the functionality of the thalamus by subtyping the part involved. The MRI scans of 83 cases were analyzed with the help of our Institution Radiologist and five subtypes could be delineated – anterior, dorsal, global, posteromedial, and posterolateral areas. The most common involvement in our series was the global type (50.6%), followed by posteromedial (18.1%), dorsal (14.5%), anterior (10.8%), and posterolateral (6%). An attempt was made to correlate the clinical features with the anatomical component of thalamus involved [Figure 3]. The important features that correlated were altered sensorium, sensory, motor dysfunction, memory disturbances, eye movement abnormalities, and gait abnormality. Abnormal gait was further subcategorized into ataxic gait, hemiplegic gait, imbalance/astasia, a combination of ataxia and hemiparesis.
Figure 3: Case 83 - MRI Brain axial showing bilateral symmetrical thalamic hyperintense signal s/o edema in T2 & FLAIR, MRI Brain axial showing bilateral symmetrical thalamic blooming signal in SWI s/o bleed, MR venogram s/o thrombosis of transverse, sigmoid sinus and internal cerebral vein. MRI = Magnetic resonance imaging, FLAIR = Fluid attenuated inversion recovery, MR = Magnetic resonanceEach clinical feature was further examined as to which part of the thalamus was the most common association thereby correlating with the anatomical substrate mostly associated with that function.
DiscussionThis was a prospective observational study of 83 patients with different thalamic lesions proven radiologically. This study tries to characterize the type of lesion, and its pathology and is an attempt to correlate with the clinical symptom that can result from that specific site of the lesion.
Imaging
There were 83 patients with radiologically proven thalamic lesions. The most common type of lesion was an infarct (52 cases), followed by hemorrhagic stroke (27), tumor (1), demyelination (1), gliosis (1), and calcific lesion (1). There is a possibility that diseases with only functional involvement or degeneration may not have been identified, for example, dementia or ASD. Patients who underwent DBS and thalamotomy were not included as these procedures were not being done in our center at the time of the study. Otherwise, earlier studies showed a similar distribution of lesions by Lee and Marsden.[25]
The unusual etiologies encountered by Jones and Rowe were migraine, thiamine deficiency, cerebral lupus, infective abscesses (fungi or toxoplasmosis), syphilitic gumma, and thalamic astrocytoma besides the commoner ischemic and hemorrhagic strokes.[36] Jones and Rowe study was mainly concentrating on ocular motility consequences of thalamic lesions.
Laterality
Unilateral lesions were more common than bilateral involvement, and among unilateral there was a slight predilection for left sided lesions in our series. Earlier studies had not suggested any side predominance. Majority of vascular lesions affect the thalamus unilaterally even though they involve vertebrobasilar circulation. Bilateral thalamic involvement is seen mostly in isolated case reports, consisting of tumours, metabolic and demyelinating diseases as described by Linn et al.[37] Our series had witnessed one patient with deep venous sinus thrombosis affecting both thalami [Figure 4]. That patient, an engineering postgraduate student, though recovered well had shown marked memory disturbances in the follow up of nearly 2 years, and could not complete his studies. Gliomas can involve both thalami, either as de novo origin from both thalami or due to contiguous spread from the contralateral side.[38]
Figure 4: Case 71. MRI Brain axial section FLAIR sequence showing left thalamus hyperintensity in view of recent h/o rapid correction of sodium lesion is s/o osmotic demyelination. MRI = Magnetic resonance imaging, FLAIR = Fluid attenuated inversion recoveryRisk factors
Considering that strokes form majority of thalamic lesions, vascular risk factors like hypertension, diabetes, smoking and hyperlipidemia are important risk factors of thalamic lesions.[37] In our study 69.9% had comorbid hypertension and 49.5% had diabetes and hyperlipidemia. In a study by Lee SH et al. (2015) the presence of systemic comorbidities strongly predicted worsening and spread of thalamic hematoma and carried poor prognosis.[38]
In general, ischemic stroke is more common in men, and when it occurs in women, women are several years older when they suffer from first stroke.[39],[40],[41],[42] In our study too, men were more commonly affected by stroke, ischemic as well as hemorrhagic. The mean age in our study was 60 years. There was one male patient who had tissue diagnosis of glioma on histopathology, and he was 22 years old. It was a bilateral thalamic lesion, and the age incidence was in line with literature as described by Menon et al., i.e., between 5 and 29 years.[38]
Clinical profile in thalamic lesions
There can be sudden appearance of contralateral sensory disturbances, pain or hypoesthesia, contralateral ataxia, weakness, and the symptoms can persist for a long time the symptoms being closely related to the region of thalamus involved.[43],[44] Motor weakness was most commonly seen following infarction or bleed, in 26 and 21 patients respectively. The motor weakness was mild on Medical Research Council scale in majority of the patients. Headache was frequently observed in bleed patients. Nausea and vomiting were also more common with hemorrhagic lesions. Sensory symptoms were more frequently seen in infarct patients, when compared to bleeds. All thalamic stroke (both ischemic and hemorrhagic) patients complained of new onset difficulty in falling asleep or of fragmented sleep. This finding is in line with other studies from literature.[45],[46],[47] One patient with a demyelinating lesion also had sleep disturbances.
A few patients complained of memory disturbances, difficulty in registration and recall of recent events. Diencephalic amnesia of different grades was described following thalamic lesions.[47],[48],[49],[50],[51],[52],[53] Many subjects had disorientation to time and date. Thalamic chronotaraxis, isolated time disorientation, was earlier described by Kumral et al. with involvement of dorsomedial and anterior nuclei of thalamus, which can last for a few days to a few months.[54]
Gait abnormality was observed in 49 patients. It was due to motor weakness, or ataxia or due to a combination of both. In two patients there was only gait imbalance without appendicular ataxia-thalamic astasia. Most commonly bleed patients had hemiparetic gait, while there was hemiparetic-ataxic (combination of motor weakness and ataxia) gait in patients with thalamic infarcts commonly. One patient with posterolateral right thalamic bleed had a peculiar type of gait as if he was pushing to the paretic side, the Pusher syndrome. This was similar to the observation of Melo and Bogousslavsky in which hemiataxia was a feature of thalamic stroke. It was likened to a “cerebellar type” of ataxia, but was almost always associated with sensory loss, also sometimes associated with motor weakness.[18] The caudal part of VL nucleus of thalamus is adjacent to medial part of the posterior limb of internal capsule. These structures are, in turn, nearer to the corticospinal pathways and ventral posterior nucleus of thalamus. Thus hemiataxia is associated with hemiparesis or hemihypoesthesia in this type of infarct.
There were no patients with asterixis or Parkinsonism or hemifacial spasm in our series.[55],[56] Twenty-three patients mostly with strokes had eye movement abnormalities in our study. Upward gaze was commonly affected, and also gave raise to pseudo lateral rectus palsy in two of our patients. The confrontation test for visual fields was defective in two of our patients, which probably was secondary to visual hemineglect.[36] These findings were consistent with other scientists' observations, which included both hemorrhagic and ischemic lesions.[57],[58]
Seizures were seen in four patients. Three were acute stroke cases, two were ischemic and one was a bleed. The seizures were of brachial onset, became faciobrachial in two patients and in one case there was secondary generalization. The seizures were well controlled with sodium valproate but lasted for nearly 1 week before complete disappearance. Literature search had shown seizures as an uncommon complication of thalamic stroke.[59] There was one patient with hypoparathyroidism with seizures for many years, uncontrolled with a variety of antiepileptic medicines. He had bilateral thalamic calcifications on imaging, and his seizures were normalized with continuous calcium infusion.
Etiological profile
All patients with unilateral thalamic lesions had stroke as the cause. But venous stroke had presented with bilateral thalamic hemorrhagic infarct in one patient. Bilateral thalamic calcification was seen in one patient with hypoparathyroidism and hypocalcemia as the cause of his refractory seizures. Rapid correction of hyponatremia was the cause of demyelination in the pons and extrapontine structures including thalami bilaterally [Figure 4].
There was one female patient who had chronic hemibody pain with insidious onset which was due to a gliotic lesion on the corresponding side in the ventrolateral thalamus on MRI imaging [Figure 5]. Thalamus is an important relay station in the transmission of nociceptive information to the cerebral cortex and can result in both acute and chronic pain syndromes.[60],[61] Astrocytoma was identified in one patient with slowly progressive ataxic hemiparesis of nearly 1-year duration [Figure 6].
Figure 5: Case 42. MRI Brain Axial FLAIR image showing gliotic area in right thalamus of patient presenting with left hemibody pain and paraesthesias. MRI = Magnetic resonance imaging. FLAIR = Fluid attenuated inversion recovery
Figure 6: Case 49. MRI Brain axial T1 post contrast scan showing right thalamic mass with nodular enhancement suggestive of glioma. MRI = Magnetic resonance imagingThough viral encephalitis due to Dengue and Japanese encephalitis are common in these parts of India, there was no such case with thalamic involvement during the preparation of this article. Similarly, we did not encounter any patient with thalamic cavernoma,[62] or thalamic onset of CJD.[63],[64]
Clinic-anatomical correlation
We tried to correlate the clinical syndrome with the part of thalamus affected by disease. Similar exercise was performed by Kumral et al.[43],[65] and Chung et al.[66] who identified the clinical syndromes due to thalamic lesions. We divided thalamus in to five parts and correlated with the clinical features.
Sensory disturbances in the form of pain and paresthesias were mostly found when thalamus was involved globally closely followed by dorsal thalamic involvement. Motor symptoms were present when posteromedial thalamus was affected. Abnormal eye movements and gaze palsies were present with global involvement. Episodic memory loss was seen with anterior thalamic lesion, and this finding was statistically significant. Other studies had also showed cognitive deficits with anterior thalamic affection.[67],[68],[69],[70] When the patient developed altered sensorium, there was global or posteromedial involvement.
The thalamic nuclei consist of five major functional classes. Reticular and intralaminar nuclei that subserve arousal and nociception, sensory nuclei represented at all domains, effector nuclei are concerned with motor function and different aspects of language, associative nuclei that participate in higher level cognitive function, and limbic nuclei concerned with mood and motivation.[71],[72] Disease processes that destroy these nuclei in different combinations can produce sensorimotor and behavioural syndromes depending on which nuclei are involved. Probably some symptoms can be explained by the mechanism of cerebral diaschisis, wherein ipsilateral thalamic blood flow decreases following acute ischemic stroke of other cerebral areas.[73],[74]
Our study highlights both common and less common clinical presentations of thalamic lesions; partial as well as globally involving the thalamus, with an attempt to correlate the clinical finding with the anatomic localization. Certain syndromes like Cheiro-oral syndrome and others are thalamic signatures in that a clear search for a thalamic lesion is mandatory with such presentation.
This study also provides insight in to the functional properties of different thalamic nuclei–the “Gateway to cerebral cortex,” which really is more than just a relay center.
ConclusionsThalamus gets involved in many systemic diseases-infective, metabolic and demyelinating conditions, and there may not be symptoms referable to thalamus in such disordersThe most common isolated thalamic lesion is an ischemic infarct with a male preponderanceThe second most common localized lesion is thalamic bleed followed by other less common pathological entitiesAmong those cases that come for clinical attention, global thalamic involvement is the most common followed by posteromedial involvementMost common clinical presentation is sensorimotor dysfunctionMemory disturbances, behavioural and cognitive dysfunction, movement disorders, sleep disturbances and seizures may also be seen, though less commonly, in thalamic disease.Author contribution
MK is mainly responsible for collecting data, RH prepared the manuscript (and guarantees the integrity of the manuscript), and BPP reviewed and corrected the manuscript.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
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