Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Paralysis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources
PubMed1999

Normokalemic thyrotoxic periodic paralysis: a new therapeutic strategy.

An unusual presentation of periodic paralysis in a Mexican man with thyrotoxicosis is presented. The patient suffered paralysis of the lower extremities without apparent precipitating factors such as hypokalemia, exercise, carbohydrate or alcohol ingestion. Hyperthyroidism was managed first with a thyroid suppressant (methimazole) and propranolol. Prednisone was added after another episode of paralysis. Definitive treatment of hyperthyroidism was achieved with radioactive iodine, which subsequently required substitution therapy with thyroxine. A moderate dose of thyroxine (100 microg) caused muscular weakness. Treatment of thyrotoxicosis and flaccid paralysis as well as the effects of glucocorticoids on thyroid function are discussed.

Adult↗
PubMed2006

Right diaphragmatic paralysis following endocardial cryothermal ablation of inappropriate sinus tachycardia.

Inappropriate sinus tachycardia (IST) is a rare disorder amenable to catheter ablation when refractory to medical therapy. Radiofrequency (RF) catheter modification/ablation of the sinus node (SN) is the usual approach, although it can be complicated by right phrenic nerve paralysis. We describe a patient with IST, who had symptomatic recurrences despite previous acutely successful RF SN modifications, including the use of electroanatomical mapping/navigation system. We decided to try transvenous cryothermal modification of the SN. We used 2 min applications at -85 degrees C at sites of the earliest atrial activation guided by activation mapping during isoprenaline infusion. Every application was preceded by high output stimulation to reveal phrenic nerve proximity. During the last application, heart rate slowly and persistently fell below 85 bpm despite isoprenaline infusion, but right diaphragmatic paralysis developed. At 6 months follow-up, the patient was asymptomatic and the diaphragmatic paralysis had partially resolved. This is the first report, we believe, of successful SN modification for IST by endocardial cryoablation, although this case also demonstrates the considerable risk of right phrenic nerve paralysis even with this ablation energy.

Catheter Ablation↗
PubMed2004

Hypokalaemia and paralysis in the Thai population.

BACKGROUND: Hypokalaemia with paralysis is a syndrome common in Thailand. This syndrome may result from hypokalaemic periodic paralysis (HypoPP), thyrotoxic periodic paralysis (TPP) or distal renal tubular acidosis (dRTA). We prospectively investigated the nature of this syndrome in afflicted Thai patients. METHODS: Blood and urine samples were collected from 47 patients during attacks for multiple biochemical and thyroid function tests. A long acid loading test was performed in all euthyroid patients. Mutation analyses were done in all HypoPP and TPP patients. RESULTS: Of the subjects, 34 completed the study. Of those, 11 (32%), eight (24%) and 15 (44%) had TPP, dRTA and HypoPP, respectively. Patients with dRTA and TPP were older than those with HypoPP. Males were more prevalent than females in HypoPP and TPP; the reverse was true for dRTA. Two-thirds of the HypoPP cases were sporadic. The majority of the HypoPP and dRTA patients resided in northeastern Thailand. Of the 11 TPP patients, nine (82%) had no previous thyroid disease. Moreover, four out of 11 patients (36%) had subtle clinical signs of hyperthyroidism; three of eight dRTA patients had renal stones, nephrocalcinosis or both. Only two patients had metabolic acidosis at the time of presentation. No common mutations were found in the HypoPP and TPP patients. CONCLUSIONS: In most of our patients, HypoPP is sporadic and not associated with the common mutations reported previously. Clinical clues that can assist in differentiating between the causes of hypokalaemia and paralysis are age at onset, gender and geographic region residence of the patients. However, the absence of previous histories of thyroid disease or overt thyrotoxicosis, and of stone disease/nephrocalcinosis or metabolic acidosis does not exclude the diagnosis of TPP or dRTA.

Adult↗
PubMed1996

Thyrotoxic periodic paralysis in a Chinese population.

We retrospectively evaluated the characteristics of adult patients admitted with thyrotoxic hypokalaemic periodic paralysis in Hong Kong. From 1984 to 1993, 45 Chinese adult patients were admitted with acute limb weakness, plasma potassium < or = 3.5 mmol/l and thyrotoxicosis confirmed by laboratory investigations. All but one were male. Seventy-five percent of attacks occurred between 9pm and 9am. Half of the attacks occurred between July and October (49.1%), most commonly in August (20%). Mean (+/- SEM) plasma potassium on admission was 2.17 +/- 0.08 mmol/l (range 1.1-3.5). In 15 episodes (27.3%), plasma potassium on recovery exceeded 5.0 mmol/l, while in three episodes (5.5%), potassium exceeded 6.0 mmol/l. No patient had a positive family history of thyrotoxic periodic paralysis. Only 28.9% had a known history of thyrotoxicosis before their first presentation with periodic paralysis. Twenty-seven (60%) had clinical evidence of thyrotoxicosis. Although all were biochemically thyrotoxic, 11.4% had only a mild degree of thyrotoxicosis (suppressed thyroid-stimulating hormone, high free thyroxine, but normal free triiodothyronine). One quarter of the patients had a normal erythrocyte zinc concentration, indicating either a short history of thyrotoxicosis or transient thyrotoxicosis. The diagnosis of thyrotoxic hypokalaemic paralysis should always be considered in Chinese patients with acute muscle weakness, especially in young males. Absence of clinical thyrotoxicosis does not exclude the diagnosis. Plasma potassium should be monitored carefully during treatment to prevent rebound hyperkalaemia.

Adult↗
PubMed2001

Hypokalaemia and paralysis.

It is not uncommon for patients to present to the emergency room with severe weakness and a markedly low plasma potassium concentration. We attempted to identify useful clues to the diagnosis of hypokalaemic periodic paralysis (HPP), because its acute treatment aims are unique. We retrospectively reviewed charts over a 10-year period: HPP was the initial diagnosis in 97 patients. Mean patient age was 29+/-1.1 and the male:female ratio was 77:20. When the final diagnosis was HPP (n=73), the acid-base state was normal, the urine K(+) concentration was low, and the transtubular K(+) concentration gradient (TTKG) was <3. In patients with thyrotoxic periodic paralysis (TPP) (n=39), hypokalaemia was very commonly accompanied by hypophosphataemia (1.9+/-0.1 mg/dl). A clinical diagnosis of sporadic periodic paralysis (SPP) was made if hyperthyroidism and a family history of HPP were both absent (n=29). One subgroup of patients with HPP had a severe degree of hypernatraemia (167+/-5.0 mmol/l, n=3). There were only two patients with familial periodic paralysis (FPP). In 24 patients, the initial diagnosis was HPP, but subsequent studies failed to confirm this diagnosis. Each of these patients had an acid-base disorder, a high rate of renal K(+) excretion in the presence of hypokalaemia, and a TTKG of close to 7. With respect to therapy, much less K(+) was given to patients with HPP, yet 1:3 subsequently had a plasma K(+) concentration that eventually exceeded 5.0 mmol/l. Using plasma acid-base status, phosphate and K(+) excretion parameters allows a presumptive diagnosis of HPP with more confidence in the emergency room.

Acid-Base Equilibrium↗
PubMed2003

Thyrotropin-secreting pituitary adenoma presenting as hypokalemic periodic paralysis.

Thyrotropin (TSH)-secreting pituitary adenoma presenting with hypokalemic periodic paralysis is extraordinarily rare and may be misdiagnosed. We describe a 44-year-old man who suffered from acute muscle weakness and inability to ambulate upon awakening in the morning. Physical examination showed hypertension, tachycardia, and symmetrical flaccid paralysis of all extremities. The major biochemical abnormality was hypokalemia (K+, 2.0 mmol/L) with low urine K+ excretion. A thyroid function study revealed elevated thyroid hormone levels and inappropriately high TSH concentrations (2.10 microU/mL). Brain magnetic resonance imaging delineated a pituitary tumor with suprasellar extension. After trans-sphenoidal removal of tumor, he became clinically and biochemically euthyroid without any further attack of paralysis. Pathological findings confirmed a TSH-secreting adenoma with exclusive TSH immunostaining. TSH-secreting pituitary adenoma must be kept in the differential diagnosis in any thyrotoxic periodic paralysis patients with detectable TSH levels to avoid delaying diagnosis and management.

Adenoma↗
PubMed2005

Skeletal muscle dihydropyridine-sensitive calcium channel (CACNA1S) gene mutations in chinese patients with hypokalemic periodic paralysis.

BACKGROUND: Thyrotoxic periodic paralysis (TPP), familial periodic paralysis (FPP), and sporadic periodic paralysis (SPP) are common causes of hypokalemic periodic paralysis and have similar clinical presentations, thus possibly sharing the identical mutations. METHODS: We analyzed the role of the three known CACNA1S gene mutations (R528H, R1239H, and R1239G) in Chinese patients, including two FPP families, 36 TPP patients, 12 SPP patients, and their relatives. Fifty unrelated healthy subjects were also studied. Genomic DNA was prepared from the peripheral blood of all patients, their family members, and healthy subjects. Mutations of the CACNA1S gene were screened using polymerase chain reaction-based restriction analysis. RESULTS: Two FPP families had the R528H point mutation, but with incomplete penetrance occurring more commonly in men than in women. Only one SPP patient had a de novo mutation (R528H). None of the TPP patients had mutations in the three hot spots. CONCLUSION: Patients with FPP have R528H mutations in the CACNA1S gene. Only a few patients with SPP may share similar mutations with FPP. TPP patients do not carry any of the three known gene mutations.

Adult↗
PubMed2003

Residual paralysis in the PACU after a single intubating dose of nondepolarizing muscle relaxant with an intermediate duration of action.

BACKGROUND: Residual neuromuscular blockade remains a problem even after short surgical procedures. The train-of-four (TOF) ratio at the adductor pollicis required to avoid residual paralysis is now considered to be at least 0.9. The incidence of residual paralysis using this new threshold is not known, especially after a single intubating dose of intermediate-duration nondepolarizing relaxant. Therefore, the aim of the study was to determine the incidence of residual paralysis in the postanesthesia care unit after a single intubating dose of twice the ED(95) of a nondepolarizing muscle relaxant with an intermediate duration of action. METHODS: Five hundred twenty-six patients were enrolled. They received a single dose of vecuronium, rocuronium, or atracurium to facilitate tracheal intubation and received no more relaxant thereafter. Neuromuscular blockade was not reversed at the end of the procedure. On arrival in the postanesthesia care unit, the TOF ratio was measured at the adductor pollicis, using acceleromyography. Head lift, tongue depressor test, and manual assessment of TOF and DBS fade were also performed. The time delay between the injection of muscle relaxant and quantitative measurement of neuromuscular blockade was calculated from computerized anesthetic records. RESULTS: The TOF ratios less than 0.7 and 0.9 were observed in 16% and 45% of the patients, respectively. Two hundred thirty-nine patients were tested 2 h or more after the administration of the muscle relaxant. Ten percent of these patients had a TOF ratio less than 0.7, and 37% had a TOF ratio less than 0.9. Clinical tests (head lift and tongue depressor) and manual assessment of fade showed a poor sensitivity (11-14%) to detect residual blockade (TOF < 0.9). CONCLUSION: After a single dose of intermediate-duration muscle relaxant and no reversal, residual paralysis is common, even more than 2 h after the administration of muscle relaxant. Quantitative measurement of neuromuscular transmission is the only recommended method to diagnose residual block.

Adolescent↗
PubMed2000

New eyebrow lift technique using a semiautomatic suturing device (maniceps) for patients with facial paralysis.

Direct browlift and the traditional fascial suspension technique sometimes leave a prominent scar above the eyebrow. Coronal browlift, mid-forehead browlift, and endoscopic browlift leave no prominent scar, but they are sometimes not suitable for patients with facial paralysis because they have been developed for rejuvenative surgery. The authors present a new browlift fascial suspension technique for patients with facial paralysis. This method uses a semiautomatic suturing device (Maniceps), which they have used to graft three fascial strips to the forehead from the fascia lata, and to suspend and lift the eyebrow with only two small incisions posterior to the hairline. The authors treated 13 facial paralysis patients, with follow-up periods of more than 6 months. The lifted eyebrows adapted to stabilized positions within 3 months. The results in all 13 patients were satisfactory, with no severe complications. This new technique is very useful because it has wide applicability, including facial paralysis patients who experience severe ptosis.

Adult↗
PubMed1988

Complete hemidiaphragmatic paralysis in a patient with multiple sclerosis.

We present a case history of a patient with definite multiple sclerosis who developed an abrupt onset of unilateral diaphragmatic paralysis, minor increase in lower extremity spasticity and complaint of marked neck stiffness. Her vital capacity during this episode was 600 mL and she was in impending respiratory failure. The diaphragmatic paralysis was demonstrated by radiographic plain films and fluoroscopy. Phrenic nerve stimulation was performed during fluoroscopy and the evoked motor response from the diaphragm recorded. There was a normal amplitude diaphragmatic twitch observed with an evoked motor response latency of 1 ms and amplitude of 300 microV. After high dose intravenous steroids, her neck stiffness and spasticity improved, her vital capacity improved to 1500 mL and her diaphragm regained its normal position and movement confirmed by followup radiographic plain films and fluoroscopy. We postulate the presence of a demyelinating plaque in the brainstem fibers descending to the phrenic nucleus as the etiology of the diaphragmatic paralysis. We are unaware of any other case reports of unilateral "upper motor neuron" phrenic nerve paralysis secondary to multiple sclerosis.

Adult↗
PubMed2000

Permanent iatrogenic vocal cord paralysis after I-131 therapy: a case report and literature review.

A patient who underwent I-131 therapy for a solitary toxic thyroid nodule subsequently experienced vocal cord paralysis, a rare complication. The patient was examined because of hoarseness 1 week after treatment. Indirect laryngoscopy at the time confirmed right vocal cord paralysis. When the examination was repeated in 6 months, no improvement was noted; vocal cord paralysis was then declared permanent. Surprisingly, 11 months after the onset of symptoms, the patient observed improvement in her voice. At 14 months, she experienced complete vocal recovery. However, a computed tomography performed after this showed that her right vocal cord paralysis was unresolved. The apparent complete recovery of her voice is believed to be a result of adaptive compensatory mechanisms. Patients who recover from hoarseness after injury to the recurrent laryngeal nerve should have cord function documented by indirect laryngoscopy or other means before the physician performs a procedure that could harm the contralateral nerve, because damage to this nerve could result in devastating consequences.

Aged↗
PubMed1984

Perceptions of a critically ill patient experiencing therapeutic paralysis in an ICU.

Prolonged therapeutic paralysis with pancuronium is commonly used in ICUs to facilitate mechanical ventilation of patients with respiratory failure. Sedation is usually given concomitantly to reduce patient discomfort, but assessment of its adequacy is made difficult by the paralysis. We recently cared for a former ICU nurse who required prolonged mechanical ventilation and paralysis and received morphine as a sedative. When she recovered, she was able to relate her experiences. She stressed the need for very frequent reorientation to time and her desire for constant explanation and re-explanation of all procedures being done by the nursing and physician staff. Her experiences provide insights that allow all ICU staff to provide better care for patients requiring therapeutic paralysis.

Adult↗
PubMed1995

Changes in acetylcholine receptor number in muscle from critically ill patients receiving muscle relaxants: an investigation of the molecular mechanism of prolonged paralysis.

OBJECTIVE: Previous reports have described prolonged paralysis after the administration of muscle relaxants in critically ill patients. The purpose of this study was to examine possible pathophysiologic causes for this paralysis by measuring muscle-type, nicotinic acetylcholine receptor number in necropsy muscle specimens from patients who had received muscle relaxants to facilitate mechanical ventilation before death. DESIGN: Prospective laboratory study of human muscle collected at autopsy. SETTING: Medical and surgical intensive care units (ICUs) at a university hospital and a research laboratory. PATIENTS: Fourteen critically ill patients, with a variety of diagnoses, all of whom required mechanical ventilatory support before their deaths in the ICU and who underwent post mortem examination. Patients were arbitrarily divided into three groups, according to their total vecuronium dose and number of days mechanically ventilated before death. Three patients were in the control group (defined as dying within 72 hrs of initiation of ventilatory support and receiving a total dose of < 5 mg of vecuronium). Six patients were in the low-dose group (defined as requiring ventilatory support for > 3 days before death and receiving a total vecuronium dose of < or = 200 mg). Five patients were in the high-dose group (defined as requiring ventilatory support for > 3 days before death and receiving a total vecuronium dose of > 200 mg). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Nicotinic acetylcholine receptor numbers as measured by specific 125I-alpha-bungarotoxin binding to human rectus abdominis muscle obtained at autopsy were determined. In general, receptor number reflected the clinical requirements for the muscle relaxants of each patient. Patients who had increasing requirements for muscle relaxants before death had increases in receptor number, as compared with control values. CONCLUSIONS: The increase in nicotinic acetylcholine receptor number in muscle from patients with an increasing requirement for muscle relaxants before death suggests that nicotinic acetylcholine receptor up-regulation may underlie the increased requirements for muscle relaxants seen in some patients. Furthermore, these findings suggest that muscle relaxant-induced, denervation-like changes may at least be partially responsible for prolonged muscle paralysis after the long-term administration of muscle relaxants. This study may provide the first information into the molecular mechanisms underlying prolonged paralysis.

Adult↗
PubMed2003

Delayed-onset facial paralysis after vestibular neurectomy.

OBJECTIVES/HYPOTHESIS: Delayed-onset facial paralysis (beginning more than 3 d after the procedure) has been described as a complication of many different types of otological procedures. The incidence of this problem in vestibular neurectomy and the relationship to surgical approach are detailed in the study. STUDY DESIGN: Retrospective case review. METHODS: In the setting of a tertiary referral center, vestibular neurectomy was performed in 70 individuals with disabling vertigo unresponsive to medical therapy who elected vestibular neurectomy. The main outcome measure was incidence of delayed onset facial paralysis. RESULTS: Delayed-onset facial paralysis was significantly more common after the middle fossa (18%) and translabyrinthine (11%) approaches compared with the retrosigmoid approach (0%). CONCLUSIONS: Surgical approach influences the incidence of delayed-onset facial paralysis. Measures to prevent this complication such as prophylactic antiviral medication or labyrinthine segment decompression may be considered in middle fossa and translabyrinthine operations.

Adult↗
PubMed1989

Outbreak of poliomyelitis-like paralysis associated with enterovirus 71.

In the summer of 1987 five children were seen at The Children's Hospital of Philadelphia because of acute onset of flaccid paralysis of an arm or leg(s). Although there were documented exposures to oral poliovirus vaccine and coxsackievirus B3 in some of the cases, the clinical, epidemiologic and laboratory findings indicate that enterovirus 71 was the common etiologic agent for this unusual outbreak of poliomyelitis-like paralysis. Of the five children three recovered completely; the other two had residual paralysis with weakness and muscle wasting. Imaging studies of the spinal cord in the two children with residual paralysis revealed defects in the ventral aspect of the spinal cord. This series of paralytic cases attributed to enterovirus 71 is the largest reported in the United States.

Child↗
PubMed1998

The effect of unilateral partial facial paralysis and muscle ablation on craniofacial growth and development: an experimental study in the rabbit.

The effect of unilateral partial facial nerve ablation and unilateral partial midface muscle ablation on craniofacial growth and development was investigated. New Zealand White rabbits (12 days old) were randomly assigned to three experimental groups: control group, to study normal craniofacial growth and development (n = 15); nerve ablation group, surgically induced unilateral paralysis of the buccal branches of the facial nerve (n = 15); and muscle ablation group, surgical unilateral ablation of the facial muscles innervated by the buccal branches of the facial nerve (n = 12). All animals were operated on at the age of 12 days; follow-up evaluations were performed at the ages of 2 months and 6 months. The age of 2 months represents the endpoint of the prepubertal craniofacial growth and development. At the age of 6 months, the animals are fully grown; therefore, the time period between 2 and 6 months is regarded as the pubertal growth period. Computerized dorsoventral roentgencephalometric (measurement of distances and angles) and computer tomographic (three-dimensional volumetric measurements) investigations were performed at both ages. Additional dry skull measurements were performed to determine more precisely the bone segments involved in the craniofacial growth alterations studied. The obtained results indicated the following. Unilateral partial facial paralysis involving the midface resulted in growth alterations analogous to those seen after unilateral total facial paralysis. The growth alterations were not to be seen as a growth restriction (reduction in bony volume) but as growth misdirections (alterations in shape). Major growth alterations were present in those regions closely related to the facial musculature, namely the nasal, maxillary, and premaxillary regions, resulting in a snout deviation toward the operated side. The growth alterations occurred during prepuberty and remained rather stable during puberty. Morphologic signs of muscle denervation were related to the craniofacial growth disturbances. The growth alterations after unilateral partial facial paralysis were mainly biomechanically induced, as they were analogous to those observed after unilateral midfacial muscle ablation. The fact that after unilateral midfacial muscle ablation at the age of 6 months the severity of the alterations had increased was attributed to the scar formation inherent to the surgical procedure.

Anesthesia↗
PubMed1999

The effect of unilateral partial facial paralysis on nasofrontal sutural growth: an experimental study in the rabbit.

In a previous study in the rabbit, it was demonstrated that paralysis of the midfacial musculature results in decreased anteroposterior growth of the snout. At the end of growth, these animals showed macroscopically striking similarities to animals with unilateral fusion of the nasofrontal suture. In this study, whether nasofrontal sutural growth is unilaterally restricted in animals with unilateral partial facial paralysis was investigated. A left-sided partial facial paralysis was induced in sixteen 12-day-old New Zealand White rabbits. At the ages of 5, 9, 12, and 17 weeks, four animals were randomly assigned to be killed for analysis of nasofrontal sutural growth. In each animal, the left experimental side was compared with the right control side. By means of histomorphometric measurements, it was shown that diminished sutural growth activity was present on the left paralyzed side in periods of rapid growth. On the other hand, no significant alterations in sutural width were found. These findings seem to explain some of the macroscopic growth alterations (i.e., diminished anterior maxillary length) observed in rabbits with unilateral partial facial paralysis.

Animals↗
PubMed1999

Effect of nerve repair after unilateral partial facial paralysis on craniofacial growth and development.

The effect of partial transection, coaptation, and freezing of the left facial nerve on craniofacial growth and development was investigated. Twelve-day-old New Zealand White rabbits were randomly assigned to four groups: control group (n = 15), nerve ablation group (n = 15) with a surgically induced partial facial paralysis, nerve coaptation group (n = 15) with a surgically induced partial facial paralysis treated by immediate microsurgical nerve coaptation, and nerve freezing group (n = 13) with a freezing-induced partial facial paralysis. All animals were operated on at the age of 12 days; follow-up evaluations were performed at the ages of 2 months (end-point prepubertal growth) and 6 months (full grown). Computerized dorsoventral roentgencephalometric analysis and computer tomographic three-dimensional volumetric measurements were performed at both ages. Roentgencephalometric analysis revealed that the growth disturbances of the nerve ablation group and the nerve coaptation group were analogous. In contrast, in the nerve freezing group, hardly any growth disturbances as compared with the control group were seen. The CT volume measurements revealed a significant left-right difference in maxillary volume at the ages of 2 and 6 months in the nerve coaptation group as compared with the control group. Muscle histomorphometric analysis revealed a shift in muscle fiber composition in the nerve coaptation group and the nerve freezing group, with an increase of type I fibers at the cost of type IIA fibers. This shift was significantly less pronounced in the latter than in the former. Nerve histomorphometric analysis revealed a significant increase in the number of nerve fibers in the nerve coaptation group as compared with the control group. In the nerve freezing group, the increase in the number of nerve fibers was not significantly different as compared with the control group and the nerve coaptation group. Both the equivalent diameter and the myelin area were equally reduced in the nerve coaptation and nerve freezing groups. Thus, the nerve coaptation group and the nerve freezing group did not differ significantly in the extent of nerve recovery, although they differed in the extent of muscle recovery. The extent of muscle recovery, in turn, was related to the extent of abnormal craniofacial growth and development. Indeed, the growth and development were hardly abnormal in the nerve freezing group and as abnormal as after untreated paralysis in the nerve coaptation group. Therefore, factors related to nerve regeneration, other than those assessed by nerve histomorphology, were considered to be responsible for these differences between both groups. The duration of the denervation time was regarded to be considerably shorter in the nerve freezing group than in the nerve coaptation group, resulting in the observed improved muscle recovery. The difference in the degree of axonal malalignment between both groups was considered to be negligible, because of the tolerance toward axonal malalignment at neonatal age.

Animals↗